SP1 and neoplasm: Many oncogenes, such as c-Myc, Sp1, HIF-1, AP-2, Estrogen receptor, and IRF1, could function as transcriptional factors to stimulate the expression of hTERT, while many tumor suppressors, such as p53, WT1, Menin and SMAD3, inhibit hTERT transcriptional activation by binding to special promoter sites [15-17].