IL-4 can induce apoptosis of AML cells in vitro and in vivo through Caspase-3 activation and STAT6 phosphorylation, and can also mediate P53-dependent apoptosis via IL-4 on LICs through the endogenous CyPG-PPARγ axis, which is a negative regulator of normal AML cells (89–91). Here, STAT6 is linked to acute myeloid leukemia.