In our study, we also found that the inhibition of histone acetyltransferase activity by CBP significantly lowered the binding of Sp1 to hTERT promoter as well as the level of acetylated Sp1, suggesting that the acetylation of Sp1 by CBP might be required to initiate the transcriptional activating mechanism of hTERT promoter in lung cancer cells. The gene discussed is SP1; the disease is lung cancer.