Targeting of either the H3K4 methylation-specific histone methyltransferase, mixed-lineage leukemia 1 (MLL1), with the epigenetic agent verticillin A, JAK/STAT pathway with ruxolitinib, mitogen-activated protein kinase (MAPK) pathway with a MAPK kinase (MEK inhibitor, cholecystokinin (CCK) receptor, DNA methyltransferase with decitabine, or Bcl-2 in combination with checkpoint blockade significantly enhanced tumor growth suppression, when compared to controls, in pancreatic cancer-carrying mouse models [19–24]. The gene discussed is SOAT1; the disease is neoplasm.