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Rejuvenation and disease reversal
Aging and many diseases share a common signature: cells occupy states they could once return from but no longer do. We ask what minimum perturbation restores a cell to a younger, more functional state.
We build large-scale functional genomics technologies to find the causal regulators of cell state — the programs that drive aging and disease, and the programs that can reverse them.
Cells move between states — the transitions that define development, and that go wrong in aging and disease. We ask what causally controls those trajectories, from the “dark proteome” of uncharacterized microproteins to genome-wide regulatory networks, and we build the high-throughput tools needed to read and rewrite them.
Aging and many diseases share a common signature: cells occupy states they could once return from but no longer do. We ask what minimum perturbation restores a cell to a younger, more functional state.
Cell state — not just cell type — is the level at which biology operates. We build a quantitative grammar of states: how they are defined, how they transition, and which transitions are reversible.
Thousands of small proteins are translated from regions once thought non-coding. We ask systematically which microproteins control cell-state transitions during aging, rejuvenation, and disease reversal.
Answering the above at scale requires new tools. We develop CRISPR, sequencing, and imaging methods that let us interrogate microproteins, translation, and state transitions in millions of cells in parallel.
Our paper on the functional landscape of non-canonical ORFs in coordinating cell fate is out in Molecular Cell.
Jin gave an invited talk at Perturb2026 (Vienna) — the first public airing of the lab’s virtual-cell effort.
Yuan-Hung Lo’s paper on large-scale CRISPR screening in primary human 3D gastric organoids is out in Nature Communications.