ENPP4 and lung carcinoma: 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.