By integrating mutation, chromosomal copy number, and clinical information, we divided CRC by the carcinogenesis step into three subgroups: (1) a hypermutated group, which includes EO-CRC with predisposing germline variants; (2) a WGD group with early TP53 mutation, genome doubling, and focal oncogene amplification leading to malignancy; and (3) a GS group, which follows conventional colorectal carcinogenesis, exhibiting point mutations in APC, KRAS, TP53, and deletion of tumor-suppressor genes. The gene discussed is KRAS; the disease is colorectal carcinoma.