KRAS and neoplasm: In GI cancers, this cascade’s constitutive activation, commonly caused by activating mutations in the PIK3CA gene [133], loss of the PTEN tumor suppressor, or overload from upstream signals like KRAS, fuels tumor progression by enabling uncontrolled proliferation, evasion of apoptosis through the inhibition of proteins like BAD and FOXO [134], and the promotion of angiogenesis and metastasis.