In brief, we found that (1) PPARγ expression is specifically upregulated in MES GSCs as well as tissues, and it is associated with poor prognosis of GBM patients; (2) biologically, PPARγ activation attenuates PMT and reduces stemness and viability of MES GSCs, which occurs mechanistically due to the suppression of the STAT3 signaling pathway; and (3) two in vivo xenograft tumor models independently confirmed the therapeutic potential of PPARγ upon pioglitazone treatment (Fig. 6). This evidence concerns the gene STAT3 and glioblastoma.