Hence, APL serves as an example of p53 dysfunction in the wildtype p53 setting, which has been well-documented in non-APL AML (211, 212) and raises the question of whether immune dysregulation secondary to inactivation of p53 pathways plays also a role in the pathogenesis of APL, and in its profound response to therapy upon the restoration of the p53-PML crosstalk. The gene discussed is TP53; the disease is acute promyelocytic leukemia.