Moreover, p53 inhibition may mitigate the theoretical risk of increasing the proportion of p53−/− mutant clones with high oncogenic potential, which are typically rare in a HSPC population from healthy donors but could be more frequent in patients with specific genetic diseases, such as Fanconi anemia or Diamond-Blackfan anemia (Lipton and Ellis, 2009; Ceccaldi et al., 2011). Here, TP53 is linked to hereditary disease.