In our research, IRF-5 showed the same tendency as the knocking down of it could increase tumor cell's resistance to cisplatin with a higher IC50, and the potential mechanism might lie on its function of secretin IFN-α, because the delivery of IRF5 protein into human primary pDCs increased IFN-α secretion [32], which has antiproliferative, differentiation-inducing, apoptotic, and antiangiogenic properties, and its clinical activity has been demonstrated in several cancers, including as post-chemotherapy maintenance [33, 34]. The gene discussed is IRF5; the disease is cancer.