The adenoma–carcinoma sequence underlies the development of CRC and involves many changes, including tumor suppressor gene inactivation (APC, TP53), oncogene activation (BRAF, PI3KA, and RAS), chromosomal instability (CIN), CpG island methylation phenotype (CIMP), and microsatellite instability (MSI) pathways [16,17]. The gene discussed is BRAF; the disease is colorectal carcinoma.