Recent studies suggest that certain tumor subtypes, such as SWI/SNF-mutant lung cancer cells (8), KRAS-driven lung and pancreatic cancer cells (9, 10), and acute myeloid leukemia (AML) cells, rely primarily on oxidative phosphorylation instead of glycolysis for proliferation and survival (11), indicating ARPC1A may promote tumor growth through this pathway. This evidence concerns the gene ARPC1A and familial pancreatic carcinoma.