The majority of CRC pathogenesis involves genetic alteration sequences of genes, like the adenomatous polyposis coli (APC) gene, which is the most common, followed by Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) and tumor protein p53 (TP53), which evolve from benign adenomas to malignant carcinomas and other molecular pathways responsible for driving tumorigenesis. The gene discussed is TP53; the disease is carcinoma.