Given that MIF-CD74 interactions are known to promote an immunosuppressive M2 phenotype in myeloid cells and facilitate immune evasion (37, 38), these results collectively demonstrate that high-RAS HSCs and GMPs may contribute to acute myeloid leukemia pathology through activation of the MIF-(CD74+CD44) axis. The gene discussed is MIF; the disease is acute myeloid leukemia.