Recent studies25,26 showed that deltarasin inhibited -PDEδ interactions by selectively binding to the prenyl-binding pocket of PDEδ with nanomolar affinity, thus suppressing oncogenic RAS/RAF signaling and inhibiting in vitro and in vivo growth of human pancreatic ductal adenocarcinoma cells that is harboring KRAS mutations. The gene discussed is RAF1; the disease is pancreatic ductal adenocarcinoma.