Thus, CtBP might contribute to tumorigenesis in estrogen-responsive tissues such as the breast and ovary due to increased NADH abundance, since CtBP is a well-known repressor of tumor suppressor genes such as BRCA1, E-cadherin, and CDKN1A/2A etc. However, from a therapeutic perspective, drugs may disrupt CtBP dimerization by depleting NADH. This evidence concerns the gene CDKN1A and neoplasm.