The evidence that these DDR enzymes support the maintenance of LSCs came from studies emphasising the critical role of ATM/ATR in the repair of DNA strand breaks, in which the inhibition of ATM or ATR kinases leads to unrepaired DNA strand breaks that trigger the myeloid differentiation of LSCs in MLLr-AML [11, 12]. The gene discussed is ATM; the disease is acute myeloid leukemia.