Through adenoviral expression of FHIT mutant alleles, we demonstrated that Fhit-substrate binding is limiting for tumor suppression, while its catalytic activity is not required for Fhit ability to trigger apoptosis [23]; moreover, we showed that the highly conserved Fhit tyrosine 114 (Y114), which can be phosphorylated by Src [24], is necessary to trigger the caspase-dependent Fhit-mediated apoptosis [25]. This evidence concerns the gene FHIT and neoplasm.