Ample evidence has proved that BRAF and MEK inhibitors could promote the priming and function of tumor infiltration T cells, facilitate antigen presentation and modulate the tumor environment to be harmful for tumor cells in mouse model and in vitro.612–617 However, the combination of CTLA-4 inhibitor, ipilimumab, with BRAF inhibitor, vemurafenib, or dabrafenib and trametinib fails for severe liver or gastric toxicity.618,619 Subsequent studies focused on the combination of BRAF/MEK inhibitors and PD-1/PD-L1 blockades, which have better tolerable safety profiles than CTLA-4 blockades. The gene discussed is CD274; the disease is neoplasm.