In vitro evidence for chemical carcinogenesis models linking carcinogen–DNA adducts to hotspots of TP53 missense mutations in human lung cancer has recently been provided (Denissenko et al, 1996), and analysis of human cancer cell deletion end points shows that the FRA3B fragile site is a common target of homologous recombination producing FHIT internal deletions (Inoue et al, 1997). The gene discussed is TP53; the disease is lung cancer.