We Cannot Build Organs Yet
That is the honest summary after thirty years of tissue engineering research and billions of dollars spent. What we can actually do right now is this. We can grow organoids that are about the size of sesame seeds. We can take organs from dead pigs, wash out all the cells, and reseed the remaining scaffold with a patient's own cells. We can bioprint biological structures at roughly the resolution of a cheap inkjet printer from 2005. These are real achievements and they have produced genuine clinical wins for simple tissues. Engineered skin, cartilage ears, bladders, cornea replacements. Real patients have real tissues they did not have before. But a transplantable whole kidney, heart, or liver is still somewhere between fifteen and thirty years away, depending on who you ask and how optimistic they feel that particular afternoon.
The gap between "miniature organ in a dish" and "functioning organ in a human body" is not a gap of incremental progress. It is a gap of fundamental unsolved problems, and most of the hype that follows this field is produced by people who either do not understand that or find it inconvenient to mention. I want to walk through where the actual problems are, because I think the honest map is more interesting than the press releases, and because understanding what is hard tells you a lot about what the next generation of work in the field needs to look like.
Organoids are genuinely revolutionary, and they are not organs
The modern organoid era has a clear origin point. In 2009, Toshiro Sato and Hans Clevers at the Hubrecht Institute took a single Lgr5-positive intestinal stem cell, embedded it in Matrigel (which is a kind of basement membrane extract derived from mouse tumor cells), added a cocktail of growth factors, and watched the cell do something almost absurd. It self-organized into a mini-gut. A small structure with crypts and villi and all the major intestinal epithelial cell types, assembled from a single starting cell. The stem cell apparently remembered how to build an entire tissue, given only the right chemical and physical context to work in. That Nature paper essentially launched a field.
Since then, organoids have been grown for nearly every organ system anybody has seriously attempted. Madeline Lancaster and Jürgen Knoblich at IMBA Vienna developed cerebral organoids in 2013 that self-organize into structures with discrete brain regions, including a progenitor zone containing outer radial glial cells found in the human brain but not the mouse. Melissa Little's lab produced kidney organoids whose nephrons segment into glomerulus, proximal tubule, loop of Henle, and distal tubule, with transcriptomic profiles matching first-trimester human fetal kidney. Sasha Mendjan's group also at IMBA created cardioids that form chamber-like cavities and contract rhythmically. The list goes on: liver organoids from Meritxell Huch at Gurdon, retinal organoids from Masayo Takahashi at RIKEN, lung, gastric, and pancreatic organoids from various groups around the world.
The clinical applications are already real, and this is worth pausing on because it is one of the few places in this post where I get to report unambiguously good news. Patient-derived intestinal organoids are used to screen drugs for rare cystic fibrosis mutations, through Jeffrey Beekman's forskolin-induced swelling assay at Utrecht. The FDA has used organoid data to approve CFTR modulators for rare variants that were previously untreatable. As of 2024, 86 clinical trials listed on ClinicalTrials.gov use organoids, most of them for cancer drug screening. Patient-derived tumor organoids predict treatment response in colorectal cancer with 84 to 93 percent accuracy, which is a level of predictive validity that traditional cell lines cannot come close to. In 2023, Yasuhiko Hirami and Masayo Takahashi published the first human retinal organoid transplant results in Cell Stem Cell, showing stable graft survival for two years in patients with retinitis pigmentosa. People who were going blind now have a graft that is still working two years later.
The newest frontier is assembloids, which is the term Sergiu Paşca at Stanford coined for multiple organoid types fused together. His team has fused cortical and subpallial organoids and watched interneurons migrate between them in real time. In 2024, Ziyuan Guo's group at Cincinnati Children's combined brain and blood vessel organoids to build the first human blood-brain barrier model. In June 2025, Oscar Abilez and Joseph Wu at Stanford published a method in Science for growing heart and liver organoids with intrinsic blood vessel networks. These are not just incremental extensions of the organoid idea, they are attempts to build the kind of multi-tissue interfaces that real organs actually depend on.
And yet. Organoids have hard limits that no amount of clever protocol optimization is going to fix. The first and most basic is the oxygen diffusion limit. Every cell in a solid tissue has to be within roughly 200 micrometers of a source of oxygen, because that is how far oxygen can diffuse before cellular consumption runs the concentration to zero. Anything thicker than that without its own blood supply develops a necrotic core. This is why organoids are sesame-seed-sized. It is not a matter of protocol, it is a fact about physics. Most organoids also lack immune cells, lack any kind of innervation, lack inter-organ communication, and stay stuck at fetal-like maturity. Kidney organoids match first-trimester transcriptomes. Brain organoids lack full cortical layering. iPSC-derived cardiomyocytes retain disorganized sarcomeres and immature calcium handling even after months in culture. Reproducibility is bad enough that in September 2025 the NIH established a dedicated Standardized Organoid Modeling Center specifically to try to address it. And the field's dirty secret is its dependence on Matrigel, which is an animal-derived, batch-variable, poorly defined material that makes clinical translation genuinely difficult. A 2025 review in Advanced Science by Wolff and Hendrix surveyed the landscape and concluded that no universal defined replacement for Matrigel yet exists.
Melissa Little herself has been refreshingly direct about this. She wrote in Stem Cell Reports in 2023 that "organoids are not organs," warning against researchers who "assume organoids are a perfect model." I think everyone in the field knows this at some level, but it gets lost in the translation to press releases, and it is worth being crisp about what organoids actually are. They are the most powerful tool we have ever had for studying how tissues self-organize from stem cells. They are not replacements for organs. They are not transplantable. They are a research platform, and the gap from research platform to clinical product is enormous.
Organs-on-a-chip solve different problems entirely
If organoids are biology left to its own devices, organs-on-a-chip are biology under engineering control. These are microfluidic devices, typically the size of a USB stick, fabricated from transparent PDMS polymer with hollow channels lined by living human cells. The key difference from organoids is the engineering. Fluid flow. Mechanical forces. Multi-tissue interfaces with controlled geometries. Rather than hoping cells figure out the right context, you build the context and put the cells in it.
The field really began with Donald Ingber's lung-on-a-chip at the Wyss Institute, published in Science in 2010. Dan Huh, then a postdoc in Ingber's lab, built a device with alveolar epithelial cells on one side of a porous membrane and endothelial cells on the other, with vacuum-driven cyclic stretching applied to mimic breathing. The mechanical stretch turned out to be essential. Without it, the cells did not properly recapitulate pulmonary edema or the inflammatory responses that characterize lung disease. This was a result that static organoid models simply could not produce, because static culture has no breath, no pulse, no shear stress, and it turns out biology cares about all of those.
The Wyss team has built more than twenty organ chip types since then, funded in part by a $37 million DARPA grant for a body-on-chips system that links ten organ types together. Their work proved its utility during COVID. Si and colleagues used the lung-on-a-chip to test antiviral compounds and showed that hydroxychloroquine was ineffective against SARS-CoV-2 while amodiaquine showed efficacy, which predicted the results of clinical trials before they came in. That is the kind of predictive validity you want from a preclinical model and that animal models frequently fail to provide.
The commercial spinoff from all this is Emulate Bio, founded around 2013 or 2014 and which has raised somewhere between $225 and $352 million depending on how you count. They ran what is still the largest organ-chip validation study ever conducted: 870 liver chips tested against 27 blinded drugs, achieving 87 percent sensitivity and 100 percent specificity for detecting drug-induced liver injury. For comparison, 3D hepatic spheroids in the same study achieved only 47 percent sensitivity. In September 2024, Emulate's Liver-Chip S1 became the first organ-chip admitted to the FDA's ISTAND qualification program, which is the regulatory pathway toward official recognition as a drug evaluation tool.
The regulatory momentum around this is real. The FDA Modernization Act 2.0, signed in December 2022, eliminated the Depression-era requirement that animal data serve as the default gateway to human trials. In April 2025, FDA Commissioner Martin Makary announced a roadmap to make animal testing "the exception rather than the norm" within three to five years. But Ingber himself wrote in Cell Stem Cell in January 2026 that organ chips "have not yet been integrated into drug-development pipelines," and a May 2025 GAO report concluded that they "will likely complement but not fully replace animal testing in the near term." The technology works. The adoption curve is slower than anyone hoped. Pharmaceutical companies are risk-averse about changing their preclinical pipelines, and organ chips have to prove themselves over and over on new drug classes before they get widely adopted.
Decellularized scaffolds: beautiful ghosts that cannot come alive
The idea behind decellularization is genuinely elegant, and I think the first time I encountered it I thought it was going to solve the whole problem. Take a donor organ from a cadaver, perfuse it with detergent through its native vasculature, wash away every cell while leaving the extracellular matrix intact, and what you are left with is a translucent ghost organ. It has the complete three-dimensional architecture of the original organ, including the entire vascular tree all the way down from arteries to capillary beds. Then you seed it with the patient's own cells and let them repopulate the scaffold. The vasculature is already there. The macro-architecture is already there. All you have to do is put the cells back.
The landmark paper was from Harald Ott and Doris Taylor in Nature Medicine in 2008. They perfusion-decellularized rat hearts using SDS detergent, reseeded them with neonatal cardiac cells, and by day 8 the constructs were generating pump function at roughly 2 percent of adult heart capacity. In 2013, Song and colleagues decellularized rat kidneys, reseeded them with kidney and endothelial cells, implanted them in rats, and observed rudimentary urine production (Nature Medicine, 2013). By 2016, Ott's group at MGH had scaled up to human cadaveric hearts, delivering 500 million iPSC-derived cardiomyocytes into decellularized human hearts and observing functional contraction under electrical stimulation.
These results sound promising if you squint, but the word "rudimentary" is doing an enormous amount of work in the summary above. Two percent of heart function is not a functional heart. Dilute urine at a fraction of physiological levels is not a functional kidney. Recellularized rat lungs achieved brief gas exchange followed quickly by edema and thrombosis. When Orlando and colleagues implanted recellularized porcine kidney scaffolds in pigs in 2012, the result was thrombi and fibrous encapsulation within days.
The killer problem with this whole approach turns out to be endothelialization of the vascular tree. Blood vessels work because they are lined, continuously and on every interior surface, with endothelial cells that produce anti-thrombogenic signals. Blood flowing past bare extracellular matrix clots almost immediately. If you want to reconnect a decellularized scaffold to a live blood supply, every single capillary has to be relined with endothelial cells at the correct density, in the correct orientation, with functional tight junctions, and the whole thing has to hold together under the hemodynamic forces of actual circulation. Relining billions of capillaries is well beyond what anyone has been able to do, and anticoagulation can only partially compensate. You end up with a beautiful ghost that thrombi the moment you connect it to a pulse.
As of early 2026, no recellularized whole organ has been implanted in a human. The approach remains at the small-animal preclinical stage. A comprehensive 2025 review in Nature Reviews Bioengineering by Saleh, Caciolli, and Giobbe, from Paolo De Coppi's group at UCL, maps the current state honestly. The scaffolds themselves are excellent. The ECM architecture really does preserve the detailed microscale geometry of the original organ. Bringing that architecture back to life is where everything falls apart, and it has been falling apart in the same place for over a decade now.
Bioprinting: reality versus hype
Bioprinting is the part of the field that gets the most press, and it is the part where the gap between hype and reality is widest, so I want to be careful. Here is where things actually stand.
There are several different bioprinting modalities and each one has its own tradeoffs. Extrusion-based bioprinting is the workhorse: you push continuous filaments of cell-laden hydrogel through a nozzle, typically at 200 to 500 micrometer resolution. It is versatile, it is relatively affordable, and the resolution is terrible compared to what real tissue needs. Inkjet bioprinting deposits tiny droplets at 50 to 100 micrometer resolution, but it can only handle low-viscosity bioinks and cannot build thick structures. Stereolithography and DLP (digital light processing) use light to photopolymerize a bioink layer by layer at 25 to 50 micrometer resolution, but this exposes the cells to UV and potentially toxic photoinitiators. Volumetric bioprinting, the newest approach, creates entire 3D structures in seconds by projecting patterned light from multiple angles into a rotating vial of photosensitive bioresin. Groups at EPFL and at UMC Utrecht (Riccardo Levato's group in particular) are pushing this rapidly, and a 2025 Nature paper introduced Dynamic Interface Printing for high-resolution support-free fabrication.
The most exciting modality specifically for organ engineering is FRESH, which stands for Freeform Reversible Embedding of Suspended Hydrogels. It was developed by Adam Feinberg's lab at Carnegie Mellon. The trick is to print soft biological materials like collagen into a gelatin microparticle support bath that holds everything in place during printing, then simply melts away at 37 degrees Celsius when the print is finished. The 2019 Science paper printed collagen heart components at neonatal scale with 20-micrometer filament resolution, including cardiac ventricles with human cardiomyocytes that showed synchronized contractions and 14 percent wall thickening during peak systole. In April 2025, Feinberg's group published CHIPS (Collagen-based High-Resolution Internally Perfusable Scaffolds) in Science Advances: perfusable channels down to roughly 100 micrometers in all-collagen constructs, with endothelial cells self-assembling into capillary-scale networks in the surrounding matrix. They built a pancreatic-like tissue construct that produced glucose-stimulated insulin release. FluidForm Bio, which is the CMU spinout, has demonstrated curing Type 1 diabetes in animal models and is planning clinical trials.
Now for the uncomfortable honesty. Exactly one bioprinted living tissue has been implanted in a human. In June 2022, 3DBio Therapeutics implanted a 3D-bioprinted ear (AuriNovo) made from the patient's own chondrocytes in a 20-year-old woman with microtia (underdeveloped outer ear). Phase 1/2a trial, 11 patients, two sites. One-year follow-up data showed successful engraftment and new cartilage formation. But ear cartilage is avascular, so no blood vessel problem, and it has basically one main cell type, which is chondrocytes. It is the easiest possible proving ground for bioprinting. And as of early 2026, 3DBio has not published peer-reviewed clinical data from this trial, which is not necessarily damning but is also not what you would expect from an unambiguously successful result.
Then there is Organovo, which should be a cautionary tale in every bioprinting investor pitch deck. Founded around 2007 as the poster child of bioprinting, Organovo promised to print functional human organs. Over the years, the company pivoted away from organ printing entirely, shifted to drug screening, sold its lead drug program to Eli Lilly, renamed itself VivoSim Labs in April 2025, underwent a 1-for-12 reverse stock split to maintain Nasdaq listing compliance, and shrank to a market cap of roughly $3.1 million. The company that was going to print your replacement heart is now a micro-cap drug screening company that changed its name so you would forget.
No bioprinted solid organ has been implanted in any human. No bioprinted solid organ has demonstrated clinically relevant function even in animal models. Headlines about "3D-printed hearts" (the Dvir group's 2019 paper from Tel Aviv is the canonical example) describe tiny heart-shaped structures, not functional organs. The heart shape is not the hard part. A medical student with a ceramics wheel can make a heart shape.
The vascularization bottleneck is the whole game
If you understand one thing about why organ bioengineering is hard, understand this. Every cell in your body has to sit within about 100 to 200 micrometers of a blood vessel. That is the oxygen diffusion limit, and it is not negotiable. Anything thicker than that without its own blood supply dies within hours to days. Your body solves this problem with a vascular tree that spans four orders of magnitude, from the aorta at about 2.5 centimeters in diameter down to capillaries at 5 to 10 micrometers, with a density so high that no cell in any tissue is ever far from oxygen. To build a transplantable organ, you need to build a vascular tree at something close to this scale and density. This is the single hardest thing in the whole field.
No current fabrication technology can print at capillary scale while building at organ scale. The best extrusion bioprinting achieves roughly 100 micrometer features. Capillaries are 5 to 10 micrometers. So there is a 10 to 20x gap at the fine end, and this is across a construct that might be 10 centimeters wide for a kidney or 15 for a heart. Two-photon polymerization can reach sub-micrometer resolution, but the fabrication time scales with the cube of volume, which makes it impractically slow for anything beyond a few cubic millimeters. You could print a capillary bed, in principle, but not for an organ. Not in any reasonable amount of time.
The field's best minds are attacking this from multiple directions. Jennifer Lewis's lab at Harvard developed SWIFT (Sacrificial Writing Into Functional Tissue), which flips the usual approach. Instead of printing the whole organ and trying to route vessels through it, you start with pre-assembled living tissue made from iPSC-derived organ building blocks, packed together at extremely high cell density, and then you print only the vascular channels into that pre-assembled tissue. The 2019 Science Advances paper packed roughly 200 million cells per milliliter and half a billion cells total, with perfusable channels at 400 micrometers to 1 millimeter in diameter. In 2024, Lewis's group published co-SWIFT in Advanced Materials, which uses coaxial printheads to create multilayered, branching vascular networks with smooth muscle cell shells and endothelial cell linings. The architecture is closer to real blood vessels than anything else that has been printed.
Jordan Miller's group at Rice University took a different approach with SLATE (Stereolithography Apparatus for Tissue Engineering), which was the cover of Science in May 2019. They used DLP stereolithography with food-dye photoabsorbers (tartrazine, Yellow #5, the same stuff in Mountain Dew) to confine the polymerization to thin layers. This let them print a lung-mimicking structure with entangled but non-intersecting vascular and airway networks. Blood flowing through the vessels picked up oxygen from a pulsating air sac. That was the first technology to demonstrate functional gas exchange through printed constructs with independent vascular networks, which is a genuinely remarkable result.
The emerging consensus is that the solution is going to be hybrid and multi-scale. Bioprinting handles macro-vessels above 100 micrometers or so, and endothelial cell self-assembly handles the capillaries below that threshold. Feinberg's 2025 CHIPS paper demonstrated exactly this architecture, with FRESH-printed channels at 100 to 750 micrometers and endothelial cells plus pericytes spontaneously forming capillary-scale networks in the surrounding collagen. This is the most convincing proof I have seen that the macro-to-micro bridge might actually be crossable.
"Might be crossable" in a centimeter-scale test construct is different from "solved at organ scale." As Mark Skylar-Scott, who co-created SWIFT and is now at Stanford, said in a February 2025 interview: "Routine use of bioprinted organs may be decades away." Feinberg himself has shifted the framing of his own work, saying: "The question is not, can we build it? It's more of, what do we build?" The fabrication capabilities are now advancing faster than our biological understanding of what the optimal vascular designs would even look like. Which means the bottleneck is not just fabrication anymore. It is partly biological knowledge.
The problems stacked on top of each other
Vascularization is the most cited bottleneck and the one that gates everything else. But if you ask researchers actively working in organ engineering what the real barriers are, you get a less tidy answer, which is that it is at least five problems stacked together and no single breakthrough solves more than one.
The iPSC maturation problem might be just as fundamental, and it gets substantially less press. iPSC-derived cells almost universally retain fetal-like phenotypes after differentiation. Cardiomyocytes have disorganized sarcomeres, immature calcium handling, and glycolytic metabolism instead of the fatty acid oxidation that characterizes adult heart muscle. Kidney organoid cells match first-trimester fetal transcriptomes. Hepatocytes show fetal gene signatures. Every strategy attempted (prolonged culture, hormonal treatment, mechanical loading, electrical pacing, fatty acid supplementation, 3D culture, nanopatterned substrates) shows some improvement but none achieves full adult maturation. The only thing that actually matures iPSC-derived cells to adult phenotypes, consistently, is implantation into an animal. Which suggests that something about the in vivo environment provides maturation cues we have not yet identified, and cannot yet reproduce in vitro.
Innervation is the sleeper problem that almost nobody talks about. A 2020 paper in npj Regenerative Medicine by Bhatt and colleagues noted that innervation has been "generally overlooked in most non-neural tissue engineering applications." But nerves are essential for cardiac function, for gastrointestinal motility, for bladder storage and emptying, for skeletal muscle maintenance, for skin sensation. Unlike vasculature, where at least some spontaneous ingrowth does happen, innervation rarely happens spontaneously in engineered tissues. Motor neurons originate in the spinal cord. Sensory neurons originate in dorsal root ganglia. Both are far from wherever you would implant an engineered organ, and you cannot just print neurons into a tissue the way you can endothelial cells, because neurons need to be connected to the central nervous system to do anything useful. A 2025 Nature Communications review explicitly argues that innervation should be "a core design element in next-generation artificial organs," which is a polite way of saying the current generation is ignoring it.
The self-organization problem may be the deepest of all. Organoids prove that cells have remarkable self-organizing capacity, given the right starting conditions. What we do not have is a sufficient understanding of what the right starting conditions actually are, or how to provide them at scale. Self-organization in organoids works at millimeter scale, produces variable and poorly reproducible structures, and cannot reliably generate the macroscale architecture (vascular trees, ductal systems, organ-level spatial compartments) that organ-level function requires. The Human Cell Atlas and spatial transcriptomics projects are beginning to map cell placement, phenotype, and interaction at organ scale, but we are nowhere near having a complete instruction set for building an organ. A 2015 NSF/Methuselah Foundation workshop ranked this problem (insufficient knowledge of how cells organize themselves) as the number one bottleneck in the whole field, above even vascularization. Ten years later, it is still the problem.
And then there is scale and manufacturing. A human heart contains about 4 billion cardiomyocytes. A kidney has around one million nephrons with more than 20 distinct cell types. Expanding billions of iPSC-derived cells under GMP conditions is itself an unsolved manufacturing challenge. 3DBio Therapeutics spent more than seven years developing their manufacturing platform just for a cartilage ear, which is the simplest possible bioengineered tissue. Apligraf, the engineered skin product that has been on the market for many years now, has a ten-day shelf life. Biological manufacturing at clinical scale is its own hard problem, independent of everything else in this essay.
What the clinical hierarchy actually looks like
The cleanest way to think about timelines in this field is as a hierarchy of difficulty, with the simplest tissues already in clinical use and complexity increasing sharply from there. Here is the honest version.
One timeline that everyone in this field should have permanently etched into their memory is the Macchiarini scandal. Paolo Macchiarini was a thoracic surgeon at the Karolinska Institute who, between 2011 and 2014, implanted synthetic tracheas seeded with stem cells into at least eight patients. He published the results in The Lancet, claiming "almost normal airways." Seven of the eight patients died. The synthetic tracheas never regenerated. Pierre Delaere, a trachea expert at KU Leuven, called the claim that a synthetic trachea could establish a new blood supply "one of the biggest lies in medical history." Macchiarini was convicted of aggravated assault by a Swedish appeals court in June 2023 and sentenced to two and a half years in prison.
The lesson from Macchiarini, which gets forgotten every time a new "breakthrough" gets announced, is that stem cells are not magic dust. Seeding cells onto a scaffold does not automatically mean they organize into functional tissue. If you bypass the hard work of proving that the seeded cells actually do what you claim they do, you are not doing medicine. You are doing something that eventually kills people and ends in a Swedish courtroom.
Where the signal is
After walking through all of this, I want to end with what I actually think is worth paying attention to in this field, because I have been mostly critical up to now and I do not want to leave the impression that nothing is happening.
The genuinely exciting developments are the ones converging on partial solutions rather than whole-organ moonshots. FRESH-printed collagen constructs with self-assembled capillary networks. The SWIFT and co-SWIFT work packing half a billion cells into perfusable constructs. Organoids being used right now, today, to screen drugs for rare diseases and predict cancer treatment response. Retinal organoid sheets surviving two years after transplantation in patients who were going blind. Organs-on-a-chip predicting liver toxicity better than animal models in blinded studies. The Stanford group growing organoids with intrinsic vasculature. These are real advances with real clinical or preclinical utility, even if none of them is "the whole heart, printed, ready to transplant."
The noise, which I would encourage you to learn to filter out, is anything claiming that whole bioprinted organs are five or ten years away. Any press release featuring a heart-shaped object that does not actually beat. Any company raising hundreds of millions of dollars on a timeline that quietly slips by a decade every few years. The Organovo trajectory should be required reading for anyone evaluating claims in this space, because it is the canonical example of how the hype cycle in bioprinting plays out over fifteen years.
The cells know how to build organs. They do it during embryonic development, reliably, from a single cell, every single time. The question for the field is whether we can learn enough about that process, and control enough of its parameters, to make it happen outside the body, at adult scale, on demand. This is not a pure engineering problem, and it is not a pure biology problem either. It is both, tangled together, and untangling them is the actual work of the next generation of researchers in this field. Anyone who tells you it is just an engineering problem is missing the biology. Anyone who tells you it is just a biology problem is missing the engineering. The people doing the actual progress are the ones who understand they have to work on both sides simultaneously.
The bottleneck is not one thing. It is vascularization and cell maturation and innervation and self-organization and immune tolerance and manufacturing and regulation, all at once. Progress on any single front is necessary but not sufficient. What makes the field genuinely interesting rather than just genuinely hard is that progress actually is happening on multiple fronts simultaneously, and the convergence of better spatial transcriptomics, better iPSC differentiation protocols, better fabrication, and better understanding of self-organization is real even if it is slow. The honest timeline is long. The direction is right. The people working on it are serious, mostly. And the destination, when we get there, is that people no longer die waiting for a kidney.