CRC commonly begins as a precancerous polyp, followed by sequential accumulation of somatic mutations that ultimately lead to malignant transformation; this adenoma-to-carcinoma sequence [176] classically begins with a mutation in the tumor suppressor APC, followed by a mutation in the oncogene KRAS, and culminates with a mutation of TP53 [177]. The gene discussed is APC; the disease is colorectal carcinoma.