KRAS, a small GTPase, cycles between a GTP-bound active state and a GDP-bound inactive state, driven by GTP hydrolysis and nucleotide exchange.494 KRAS mutations are among the most common oncogenic alterations in cancer,495 leading to the constitutive activation of downstream pathways such as MAPK and AKT-mTOR, which are crucial for cell proliferation and survival. This evidence concerns the gene KRAS and cancer.