It is possible that the recurrent involvement of FHIT in RCC‐associated chromosome 3 rearrangements reflects the presence of palindromic AT‐rich repeats at the t(3;8)(p14.2;q24.1) breakpoint and causes a propensity to recurrent rearrangements at this locus,54 although we note that only a fraction of chromosome 3 translocations are associated with predisposition to RCC.55 It is therefore conceivable that both instability of the translocated chromosome and monoallelic inactivation of FHIT contribute to RCC susceptibility. The gene discussed is FHIT; the disease is renal cell carcinoma.