The rat sarcoma virus (RAS) superfamily members, including HRAS, KRAS, and NRAS in mammals, play significant roles in the pathogenesis of various human cancers.1 Notably, KRAS is commonly mutated, contributing to the activation of this gene in a multitude of cancer cases, including 80% to 90% of pancreatic cancers, 40% to 50% of colorectal cancers, and 30% of non-small cell lung cancers.1 However, the clinical therapeutic options are considerably constrained for individuals harbouring KRAS mutations. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.