KRAS and colorectal cancer: Colorectal cancer (CRC) arises through a multistep adenoma–carcinoma sequence initiated by the accumulation of oncogenic mutations (e.g., loss of the APC tumor suppressor gene leading to constitutive Wnt/β-catenin signaling), followed by the activation of alterations in KRAS and inactivation of TP53, which together drive aberrant crypt formation and uncontrolled proliferation in the colonic epithelium [9,10,11].