In the primary human ovarian cancer cells (“pOC-1/-2/-3/-4”), shBRDT-3-induced BRDT silencing (see Fig. 2) resulted in caspase-3 activity increase (Fig. 3F), mitochondrial depolarization (JC-1 green monomers accumulation, Fig. 3G) and apoptotic nuclei increase (Fig. 3H), confirming apoptosis activation. This evidence concerns the gene BRDT and ovarian cancer.