TNF-α primarily exerts its biological effects through its interaction with two surface receptors—TNFR1 and TNFR2—activating downstream signaling cascades such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK), which are often aberrantly regulated in high-grade gliomas [4,5,6,7]. This evidence concerns the gene TNF and glioma.