It has been demonstrated that the catalytic activity of endogenous HDAC3 requires the interaction with DAD domain of either the NCOR1 or SMRT [170] and, according to their biological function as a complex, NCOR1, SMRT, and HDAC3 have been observed to be upregulated in numerous types of cancer including colon, lung, prostate, and breast cancers. The gene discussed is NCOR2; the disease is breast cancer.