In conclusion, a pro‐GBM mechanism in which CYP2E1‐PPARγ‐STAT‐1/NF‐κB/STAT‐3/STAT‐6 axis fueled tumorigenesis by reprogramming M/Mφ and Q11 as a promising anti‐inflammatory agent for GBM treatment is uncovered. The gene discussed is NFKB1; the disease is glioblastoma.