It is also possible that the yeast ham 1 mutant hypermutability maybe a very special case, because yeast possess neither a molybdenum cofactor-dependent pathway of HAP destruction [62], [63], nor Endo V. Elevated levels of DNA breaks and the increase in HAP-induced mutant frequencies observed in the case of ITPA knockdown provide a possible link between ITPA deficiency and a predisposition to therapy-related and spontaneous cancer caused by intrinsic base analogs. The gene discussed is ITPA; the disease is cancer.