RAD50 and cancer: CtBP-interacting protein (CtIP) is a key rate-limiting component of HR repair that interacts with the Mre11/Rad50/Nbs1 (MRN) complex to promote DSB end-resection, generation of ssDNA tails, and initiation of DSB repair.4 While ATM and CtIP are indisputably important mediators of cancer resistance to genotoxic agents, efforts to reduce cancer cell resistance to therapy via directly targeting these molecules are inherently limited given their essential functions in normal cells.