Forthcoming reports may yield insight as to whether favorable risk AML subgroups, currently defined in genetic terms, are enriched for a favorable immune profile as complement, as one might imagine for NPM1-mutated AML with wildtype FLT3. By comparison, the current high-risk genetic subgroups of AML may have in common the enrichment of a suppressive immunologic milieu supported by non-cell autonomous mechanisms as has been suggested for FLT3-ITD. This evidence concerns the gene NPM1 and acute myeloid leukemia.