In our published work, we have demonstrated that targeting the interaction of Mad1 with the PAH2 domain of Sin3A using a small molecule inhibitor (SMI) confers retinoid sensitivity in triple negative breast cancer cells (TNBC) by upregulating the expression of RARα and RARβ and by increasing retinoic acid metabolism in TNBC [20]. The gene discussed is SIN3A; the disease is triple-negative breast carcinoma.