These mutations result in a new consensus binding site for E-twenty-six (ETS) transcription factors and this may contribute to increased TERT. The ETS transcription factors are downstream targets of the RAS-RAF-MAPK pathways, and TERT promoter mutations are suggested to have synergistic effects with activating BRAF or NRAS mutations to promote tumor cell proliferation [21]. This evidence concerns the gene TERT and neoplasm.