Several studies have demonstrated that transient inhibition of p53 decreases the DNA damage response and increases HDR levels [89,98,159], but further work is required to evaluate the safety of using such inhibitors, given the tumor suppressive function of p53, in a setting where even target-specific DSB-dependent editing events contribute to hematopoietic abnormalities [46,47,48,49,266]. The gene discussed is TP53; the disease is neoplasm.