Since NHEJ and HR are the predominant DSB repair pathways, several studies have been devoted to the design of specific small molecule inhibitors targeting key proteins in the two pathways, such as ATM, ATR, Chk1/Chk2, poly (ADP-ribose) polymerase (PARP), and RAD51 inhibitors.78 Chk1/Chk2 inhibitors could act as sensitizers to radiation and DNA-damaging drugs, such as irinotecan and gemcitabine, and enhanced response in mouse tumor models.91–93. This evidence concerns the gene RAD51 and neoplasm.