In general, this precursor lesion can follow two major pathways: (i) the traditional adenoma–carcinoma pathway (70–90% of CRC cases) that begins upon APC mutation, followed by RAS activation or TP53 loss of function, or (ii) the serrated neoplasia pathway (10–20% of CRC cases), which is associated with RAS and RAF mutations and a CpG island methylation phenotype, leading to either microsatellite stable or unstable cancers [33]. The gene discussed is TP53; the disease is colorectal carcinoma.