Preneoplastic lesions undergo gradual accumulation of genetic and epigenetic changes that inactivate suppressor genes, such as TP53, adenomatous polyposis coli (APC), and SMAD family member SMAD 4 (SMAD4) and activate tumour pro-oncogenes, such as the Kirsten rat sarcoma viral oncogene homolog (KRAS) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), that provide selective proliferation advantages and induce CRC progression [5]. The gene discussed is APC; the disease is neoplasm.