I joined the Institute of Molecular Biology, Academia Sinica, as an Assistant Research Fellow in January 2026. I received my PhD from the National University of Singapore in the laboratory of Dr. Daniel Tenen, where I studied the roles of transcription factors and histone lysine acetyltransferases in hematopoiesis and acute myeloid leukemia. I then completed my postdoctoral training in the laboratories of Dr. Dieter Söll at Yale University and Dr. Brian Liau at Harvard University. During my postdoc, I developed and applied mutational approaches to investigate the functions of chromatin regulatory complexes in cancer.

My laboratory seeks to uncover how chromatin factors shape gene regulatory programs. Histones and chromatin regulators are central components of these process and are among the most frequently mutated proteins in cancer. Despite their importance, many of these proteins have diverse functions, yet the molecular mechanisms underlying their activities remain poorly understood. 

To address this challenge, we combine functional genomics, mutagenesis, and mechanistic studies to interrogate protein function at unprecedented scale and resolution. Using CRISPR-based endogenous mutagenesis and other genetic approaches, we systematically identify the protein regions and molecular interactions required for function. We integrate cellular, genomic, and biochemical approaches to uncover mechanisms by which chromatin regulators control gene expression and how their disruption contributes to disease. Our goal is to identify therapeutic vulnerabilities and translate these discoveries into new cancer therapies.

Chromatin regulators and histones constitute the fundamental machinery that governs access to the genome. Notably, genes encoding these factors are among the most frequently mutated in human cancer. A particular focus of our research is understanding how mutations in histone lysine methyltransferases and histones rewire chromatin regulation to drive tumorigenesis. More broadly, we seek to uncover the molecular mechanisms by which chromatin-associated factors regulate gene expression and how their disruption contributes to disease. By integrating functional genomics with mechanistic studies, we investigate how altered chromatin regulation gives rise to pathological states. We aim to connect genetic variation to molecular mechanisms and cellular phenotypes, thereby identifying actionable vulnerabilities that can be exploited for cancer treatment.