The mechanism by which a regular dose of aspirin inhibits tumorigenesis can be explained by the results of immunohistochemical staining that epidermal growth factor receptor (EGFR) and cyclooxygenase‐2 (COX‐2) are concomitantly overexpressed in epithelial cells of the colorectal polyps of FAP patients, but that both overexpressions are attenuated by a regular dose of aspirin.34 The gene discussed is FAP; the disease is polyp of large intestine.