It remains to be seen whether p53 inactivation or mutation in AML recapitulates the non-cell autonomous mechanisms observed in epithelial tumor models leading to increased inflammatory cytokines and M2-macrophages associated with disease initiation and progression or whether impaired regulation of TLR signaling and interferon pathways is implicated in the initiation or maintenance of TP53-mutated AML. Here, TP53 is linked to acute myeloid leukemia.