A pro‐GBM mechanism in which CYP2E1‐PPARγ‐STAT‐1/NF‐κB/STAT‐3/STAT‐6 axis fueled tumorigenesis by reprogramming M/Mφ and a newly developed CYP2E1 inhibitor, Q11, as a promising anti‐inflammatory agent for glioblastoma treatment is uncovered. This evidence concerns the gene STAT6 and glioblastoma.