The ability of calystegines to promote cell viability was closely related to a significant repression of the apoptosis genes’ transcription (p53, p21, Bax) and, more interesting, to the restoration and upregulation of the cell survival gene Bcl2. Apoptosis is known to play a pivotal role in the pathogenesis processes of various diseases, including metabolic syndrome [32]. This evidence concerns the gene BCL2 and metabolic syndrome.