Paradoxically, examination of cells that have lost the FHIT gene product has revealed that Fhit protein has functional roles in response to DNA damage [13]: 1) kidney epithelial cells established from Fhit−/− mice exhibited >2-fold increased chromosome breaks at fragile sites vs corresponding Fhit+/+ kidney cells [14]; 2) the frequency of mutations following replicative or oxidative stress in Fhit-deficient transformed and cancer cells was 2 to 5-fold greater than in Fhit-expressing cells [15], [16]. This evidence concerns the gene FHIT and cancer.