A preclinical study showed that BRAF/MEK-targeted therapies had effects, such as enhancing intratumor T-cell infiltration, increasing tumor antigens, and increasing the expression of programmed death-1 (PD-L1), on the tumor microenvironment, which supported their combination with PD-1/PD-L1 inhibitors (17–19). The gene discussed is CD274; the disease is neoplasm.