Moreover, SMYD3 regulates the transcription of hTERT, a major control factor of tumor cell immortalization, through its binding to two responsive sites on the promoter of hTERT. SMYD3 deficient tumor cells lose occupancy of the hTERT promoter by the transcription factors c-MYC and Sp1, leading to repression of telomerase activity [60]. This evidence concerns the gene SP1 and neoplasm.