KRAS is a critical oncogene encoding a GTPase that regulates cell proliferation and serves as a key driver in human cancers 1. The protein functions as a molecular switch, binding GDP/GTP with intrinsic GTPase activity, and activates downstream signaling pathways including MAPK1/MAPK3, ultimately affecting cell growth and survival 2. KRAS mutations occur in approximately 11-14% of all human cancers, making it one of the most frequently mutated oncogenes 3. The most common mutations include G12D (44%), G12V (34%), and G12R (20%) in pancreatic cancer, with G12C prevalent in lung adenocarcinoma 4. Mutant KRAS drives oncogenic transformation through multiple mechanisms, including activation of mitochondrial biogenesis via MYC induction and cooperation with other oncogenes like ARF6 for immune evasion 5. KRAS mutations frequently co-occur with TP53, PIK3CA, and APC mutations in a cancer-type-specific manner 6. Clinically, KRAS represents a major therapeutic target, with recent development of mutation-specific inhibitors like KRAS G12C inhibitors showing promise, while G12D-targeted therapies are entering clinical trials 78. The protein's central role in cancer initiation and maintenance makes it crucial for understanding tumor biology and developing targeted therapies.