We are the Kim Lab for 3D Genome and Disease Mechanisms. We map how two meters of DNA fold inside a single nucleus, and how that architecture drives cell identity, development, and disease.
Every cell in your body carries the same genome — yet a neuron, a T cell, and a tumor cell behave nothing alike. A major reason is how the DNA is folded. That 3D architecture decides which genes meet their switches. We study the rules of that folding, and what breaks when disease takes hold.
Structural proteins like CTCF and cohesin pull DNA into loops and neighborhoods (TADs), bringing distant genes and their regulators into contact.
Cutting-edge molecular tools plus next-generation sequencing turn invisible 3D contacts into high-resolution maps (Hi-C) we can read, compare, and model.
By reshaping folds on purpose, we test cause and effect — and look for ways to steer gene expression and cell identity toward health.
This is the heart of what we study. A genome can carry no new mutation in a gene itself — yet still drive disease, simply because the 3D fold around that gene has changed. Here is the chain we trace, step by step.
A loop keeps each gene paired with the right regulatory switch. The cell behaves normally.
A broken boundary lets the wrong switch hijack the gene — turning it on or off at the wrong time.
With its genes misfiring, the cell loses its identity — the root of cancer and other disease.
Folding errors are linked to many diseases — cancer, leukemia, medulloblastoma, schizophrenia, fragile X syndrome, immune dysregulation and metabolic disease. Because the fold — not always the gene — is what's broken, it may also be reversible. That possibility is what drives our lab.
Three active directions, from disease mechanism to engineering the genome itself.
Infection, nuclear stress, and other insults reshape the genome — SNPs, copy-number changes, structural variants — that drive cancer. We build 3D folding maps of cancer samples with unstable genomes to uncover the mechanisms behind these changes and their clinical meaning.
Every day our DNA is broken and repaired — never on bare DNA, but on DNA folded into a 3D structure. How that fold reorganizes around a break, and whether it helps or hinders faithful repair, is poorly understood, yet errors here are a root cause of cancer. We map how folding shifts at damage sites and ask what happens when repair goes wrong.
The genome is organized in a hierarchy — loops, TADs, compartments, chromosomes. How domains form, and how loops cause changes in transcription, is still elusive. We are building new technology to reshape folding domains on demand and test their function at target genes.
Real progress on the 3D genome needs the bench and the keyboard talking to each other. You can join from either side — and grow into both.
A 6-minute walkthrough of the lab's core ideas — how 3D genome folding shapes gene expression, how it goes wrong in disease, and what we're building to read and rewrite it.
Trained across four countries and the pharma industry — from chromosome biology in Melbourne, through Bill Earnshaw's lab in Edinburgh, to Charles Lee's lab at the Jackson Laboratory and Jennifer Phillips-Cremins' genome-folding lab at Penn, then GlaxoSmithKline, now building a lab at KAIST.
The 3D genome is one of biology's newest frontiers — most of its rules are still unwritten. We are early enough that the questions are wide open, and small enough that what you do actually matters. This is a rare window.
In a growing lab, you own a real question — not a fragment of someone else's. You'll design experiments, hit walls, and find your way through.
Come in from the bench or the keyboard — and leave fluent in both. Wet-lab biologists learn to read genome-folding data; computational students learn what the cells are actually doing. That combination is rare and sought-after.
The PI brings the playbook from Melbourne, Charles Lee's lab at the Jackson Laboratory, and Jennifer Phillips-Cremins' lab at Penn — to a lab embedded in KAIST's medical-science ecosystem.
We engineer genome folding that didn't exist before, and chase disease mechanisms no one has mapped. The frontier is unclaimed — and the early members help define what this lab becomes.
Most of our members arrive having never touched the 3D genome. We don't expect a finished scientist — we expect curiosity, persistence, and the nerve to sit with a hard problem. The rest, we build together.
Medicine, biology, bioengineering, computer science. If the 3D genome makes you curious, we want to hear from you.
Self-motivated students across all disciplines. The starting point for a Ph.D. in 3D genome biology.
Highly motivated researchers ready to lead a project. Reach out with your CV and interests.
Molecular biology, genomics, genome engineering, and cell biology wet-lab roles.
Strong Python experience and a hunger to find biological meaning in genome-folding data.