The Cancer Genome Atlas Research Network reported that the KRASWT tumors had significantly elevated tuberous sclerosis complex/mammalian target of rapamycin (TSC/mTOR) signaling pathway activity compared with KRAS mutant tumors, indicating that functional activation of the mTOR signaling pathway may be an alternative oncogenic driver in KRASWT pancreatic cancer (15). This evidence concerns the gene KRAS and familial pancreatic carcinoma.