Moreover, APL treatments also activated PPARγ, whereas pretreated with GW9662, a specific inhibitor of PPARγ, or blocking PPARγ using RNA interference could notably inhibit APL-induced PPARγactivation which resulted in a consequence of weakening APL-induced up-regulation of FGF21 and p-AMPK expressions and decreasing APL-induced a increase in glucose uptake capacity of palmitate -treated L6 myotubes. This evidence concerns the gene FGF21 and acute promyelocytic leukemia.