We then introduced a C228T mutation in the telomerase reverse transcriptase (TERT) promoter region to create a genetic background that promotes rapid tumor progression through reactivation of the TERT gene, a characteristic of GBM progression due to binding of E‐twenty‐six (ETS) transcription factors that may be coordinated by a heterotetrameric GABP transcription factor complex or non‐canonical NF‐κB signaling.[8, 13]. The gene discussed is NFKB1; the disease is neoplasm.