A series of studies on the role of acetyl-CoA in pancreatic cancer has revealed that KRAS mutations in pancreatic cancer mediate the production of acetyl-CoA, which subsequently upregulates the expression of oncogenes through histone acetylation, thereby promoting the development of pancreatic cancer (7, 8), emphasizing the crosstalk between nonmutational epigenetic reprogramming and cellular metabolism. Here, KRAS is linked to familial pancreatic carcinoma.