For example, overexpression of miR-17-92 can directly target TRAF3 to upregulate the NF-κB signaling pathway in gastric cancer; RIP2 has been identified as a new binding partner of TRAF3 in glioma and is involved in the regulation of NF-κB, and knocking down RIP2 can increase TRAF3 expression; and deletion of TRAF3 and CYLD in head and neck squamous cell carcinoma can activate NF-κB [57–60]. This evidence concerns the gene CYLD and central nervous system cancer.