The authors suggested this pathogenesis sequence is stimulated by a series of mutations in a number of oncogenes and tumor suppressors, such as the adenomatous polyposis coli (APC) gene, in the initial step of transforming normal epithelium into early adenoma, followed by the accumulation of other gene mutations, such as KRAS, TP53, and loss of heterozygosity 18q, in the subsequent carcinogenic steps. The gene discussed is APC; the disease is neoplasm.