Although different KRAS alleles (e.g., G12C vs. G12V) can exhibit distinct signaling biases,48,49 comprehensive multi-omics profiling has conclusively demonstrated that co-mutations in STK11, TP53, and CDKN2A/B, rather than the specific KRAS mutation subtype itself, serve as the principal architects of biological heterogeneity and therapeutic response in KRAS-driven cancers.50 This evidence concerns the gene TP53 and cancer.