A study from MD Anderson identifies DPY30 as a key epigenetic regulator linked to genomic stability under DNA replication stress in pancreatic tumors. Researchers at The University of Texas MD Anderson Cancer Center reported DPY30 plays an indispensable role in maintaining genomic stability during replication stress in pancreatic tumors. The discovery expands understanding of pancreatic cancer biology and opens a potential route to enhance tumor responsiveness to immunotherapy. By targeting the replication-stress vulnerability, the work adds a new biology-driven lever that could be combined with existing immunotherapy approaches in a disease area where durable responses remain limited.