KRAS is a proto-oncogene encoding a GTPase that plays a central role in cellular proliferation and oncogenesis. The protein binds GDP/GTP and possesses intrinsic GTPase activity, regulating cell proliferation through activation of MAPK1/MAPK3 signaling pathways. KRAS mutations are the most commonly mutated oncogene in human tumors, occurring in a quarter of all human cancers 1. The protein promotes oncogenic events by inducing transcriptional silencing of tumor suppressor genes in colorectal cancer cells and drives constitutive macropinocytosis in pancreatic cancer cells through PI3Kα and RAC1 activation 2. KRAS mutations are particularly prevalent in pancreatic ductal adenocarcinoma (up to 90%), colorectal cancer, and lung adenocarcinoma, with G12D being the most common variant (44% in pancreatic cancer) followed by G12V and G12R 3. These mutations drive tumor initiation and maintenance through sustained proliferation and survival signaling. Clinically, KRAS represents a high-priority therapeutic target with recently developed covalent inhibitors showing promise. Sotorasib and adagrasib target KRASG12C mutations and have demonstrated clinical efficacy in non-small cell lung cancer, while MRTX1133 targeting KRASG12D has entered clinical trials for pancreatic cancer 3. However, intrinsic and acquired drug resistance frequently occurs, highlighting the need for combination strategies and next-generation inhibitors targeting the most prevalent KRAS mutations.