PDAC often harbors the universal mutations in the proto-oncogene K-RAS (>90% prevalence in pancreatic cancer), which persistently accelerates and activates various oncogenic events (e.g., uncontrolled proliferation, sustained angiogenesis, metastasis, or invasion), thus leading to metabolic reprogramming and resistance to cell death [1, 2]. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.