Given that targeting the interaction between p53 and MDM2/MDMX through small-molecule inhibitors has not been a widely tested strategy for overcoming tumorigenesis of p53 wild-type tumors [122], exploring the anti-leukemic efficacy of potential combinatorial strategies between autophagy modulators and MDM inhibitors for the treatment of AML harboring wild-type p53 protein presents a challenge. Here, TP53 is linked to acute myeloid leukemia.