Although the three cases of AML post-cytotoxic therapy, harboring a RUNX1 copy number gain (all cases), a complex karyotype (in two cases), and TP53 mutations (all cases), likely have a different underlying pathobiology, their presentation with a mixed-lineage phenotype is worth mentioning here in order to consider AML with a RUNX1 lesion, associated with aberrant B-cell expression, in the differential versus the diagnosis of an MPAL-B/myeloid. This evidence concerns the gene RUNX1 and acute myeloid leukemia.