KRAS and neoplasm: The hyperactivation of oncogenes (e.g., KRAS) and the downregulation of tumor suppressor genes (e.g., TP53 and CDKN2A) promote tumor progression through the activation of various signal transduction pathways, including Wnt/Notch, c-Jun N-terminal kinase (JNK), PI3K, KRAS, and transforming growth factor (TGF)-β.