The results revealed that both wild-type and hydrolase-dead mutant FHIT successfully reduced the BRCA1 and RAD51 protein levels in FHIT−/− lung cancer cells (Supplementary Fig. 8b), suggesting that the Ap3A hydrolase activity of FHIT is not crucial for HRR protein stability or DNA damage repair signaling. Here, RAD51 is linked to lung cancer.