Promutagenic lesions resulting from depurination of aflatoxin–nucleoside adducts are susceptible to faulty repair, causing G to T transversions, which have been shown to result in inactivation of the TP53 tumor-suppressor gene in aflatoxin-associated hepatocarcinoma (Kensler et al. 2003). The gene discussed is TP53; the disease is neoplasm.