KRAS and pancreatic neoplasm: Consistent with the concept of PI4P/PS exchange for the enrichment of PS in the PM, pharmaceutically inhibiting a class III PI4P kinase, PI4PKIIIα, via a specific PI4PKIIIα inhibitor Compound 7 (C7), compromised the spatiotemporal organization of GFP-KRASG12V on the PM, and reduced the colony number of the mutant KRAS-dependent pancreatic tumor cells in colony counting assays [80].