By using a GEMM driven by KRASG12D mutation and homozygous TP53 loss, a recent study demonstrated that inhibition of cholesterol biosynthesis with statins, a widely used inhibitor of the mevalonate pathway, or NAD(P)-dependent steroid dehydrogenase-like enzyme inhibitor can switch glandular pancreatic carcinomas to a basal phenotype.202 Loss of function of TP53 can drive tumorigenesis via downregulation of cholesterol transporter gene ATP-binding cassette subfamily A member 1 and activation of PI3K/sterol regulatory element-binding protein 2 (SREBP2) maturation. The gene discussed is TP53; the disease is exocrine pancreatic carcinoma.