These pathways are associated with certain combinations of major molecular features of CRC, including microsatellite instability (MSI), the CpG island methylator phenotype (CIMP), and somatic mutations in BRAF and KRAS. The “conventional” adenoma-carcinoma pathway is characterized by non-MSI-high and CIMP-low or negative, and no mutations in BRAF or KRAS; the “serrated” pathway by frequent mutation in BRAF and CIMP-high; and the “alternate” pathway by KRAS mutation and non-MSI-high or CIMP-low or negative (1–3). Here, KRAS is linked to adenoma.