Furthermore, a low BCL2/BAX ratio was revealed, thus inhibiting apoptosis.[9] Another in vitro study demonstrated that silencing of CGB genes induces apoptosis in cervical cancer cells.[10] The anti-apoptosis effect may be exerted by transforming growth factor β1 in cancer cells.[11] Furthermore, overexpression of hCG promoted the proliferation of ovarian epithelial T29 and T80 cell lines in vitro, as well as increased G2 cell populations and elevated expression of cyclin E, cyclin D1, and cyclin-dependent kinases 2, 4, and 6, thus regulating the progression of the cell cycle.[12]. This evidence concerns the gene BCL2 and cervical carcinoma.