The chemical inhibition of DNMT3B with adriamycin and azacytidine reduced human TERT (hTERT) expression and, in changing GC to AT, abolished promoter activity through site-directed mutagenesis in glioma cell lines, demonstrating that DNMT3B and GC islands in the TERT promoter play an important role in the regulation of telomerase expression [12,32]. The gene discussed is TERT; the disease is central nervous system cancer.