CRC pathogenesis involves two distinct precursor pathways: the adenoma-carcinoma pathway, characterized by chromosomal instability (CIN) and accounting for 60–70% of cases (17), which typically initiates with APC mutations followed by RAS activation or TP53 functional loss; and the serrated neoplasia pathway, associated with KRAS and BRAF mutations and epigenetic instability, leading to both microsatellite-stable (MSS) and microsatellite instability (MSI) CRC. Here, KRAS is linked to neoplasm.