For example, a recent study reported ATR inhibition led to synthetic lethality in ATM-defective CLL cells.43 Another work showed that the PARP1 inhibitor, olaparib, selectively killed ATM-deficient lymphoid tumor cells.44 Interestingly, one group found that ATM-defective cells displayed strong non-oncogene addiction to DNA-PKcs (DNA-dependent protein kinase catalytic subunit), and that these cells underwent apoptosis after exposure to DNA-PKcs inhibitors.45 This evidence concerns the gene PRKDC and lymphoid neoplasm.