Interestingly, in human cervical carcinoma SiHa cells TQ induced apoptosis, arrested cell cycle at the sub-G1 phase, by modulating p53 and Bcl2 expression, decreased proliferation, reduced GSH levels and increased MDA concentration, without cytotoxic effect on normal cells (3T3-L1 and Vero cells) [71,72], while in human cervical carcinoma C33A cells TQ promoted apoptosis by activating caspase 3 [73]. This evidence concerns the gene BCL2 and cervical carcinoma.