A signal is only as meaningful as the cell that reads it. Growth factors, cytokines, and metabolic cues never act alone. Each cell receives them through its own regulatory layers, a resident transcription factor network and chromatin state, and these decode the input and build the machinery that reaches the genome.

No two cell states read alike. One signal is refracted into many programs of gene expression. Yet the opposite is just as striking. In different contexts, distant cells can converge on the same program, as when metastatic or therapy-resistant cells co-opt the transcriptional logic of development and regeneration. The signal proposes. Context decides.

This is what drives cell state transitions. As the chromatin landscape shifts, familiar signals are read anew. Cells are pushed from one identity into another, and a tissue is repaired, remodeled, or transformed.

We work to crack this code: how context gives signals meaning, how cell states hold their identity, and how its failure drives disease.