The latter publication reporting the counterintuitive finding that Phf6 loss reduces AML growth and stemness contradicts the model of PHF6 as a leukemia suppressor; however, the publication’s use of fusion protein drivers that do not co-occur with human PHF6 mutations may indicate that the chosen AML models recapitulated narrow disease subsets potentially not reflective of broader AML biology. This evidence concerns the gene PHF6 and acute myeloid leukemia.