Another possible target for the treatment of human APL is represented by the ILC2–MDSC axis, mostly driven by ILC2-produced IL-13: blocking any steps of this axis reversed the immunosuppression and significantly prolonged the survival time in humanized leukemic mice, while treating APL with retinoic acid reversed the increase in ILC2-induced MDSCs, as well as tumor- and ILC2-derived factors, in human patients with APL [32]. Here, IL13 is linked to neoplasm.