The results show that low-dose TNF-α (10 ng/mL) significantly promotes GBM cell malignant phenotypes and lipid droplet accumulation via the Tumor Necrosis Factor Receptor (TNFR) signaling pathway, a process dependent on its downstream adaptor protein, Tumor necrosis factor receptor-associated factor 2 (TRAF2). This evidence concerns the gene TNFRSF1A and glioblastoma.