The TERT promoter mutations can produce new E-26 transcription factor binding sites, promote transcription, and thus increase activity.115 Interestingly, the combination of the E-26 transcription factor and the mutant TERT promoter is not enough to drive its transcription, but this process requires the non-canonical NF-κB signaling to stimulate a response, and continuous telomerase activity, leading to cancer progression.116 TERT promoter mutations are very common in the GBM of IDH-wt.84 However, in the current clinical trials, it has not been studied as a target for GBM therapy. Here, NFKB1 is linked to glioblastoma.