Researchers reported that loss of the epigenetic regulators KMT2C/D creates targetable vulnerabilities in cancer. The work connects tumor dependency to COMPASS-related biology, focusing on how disruptions in Set1-associated methyltransferase complexes can reshape differentiation programs and growth behavior. The study frames KMT2C/D loss as a mechanistic entry point for targeted therapeutic development, supporting the broader trend of mapping context-specific epigenetic weaknesses in solid and blood cancers.