It relies on a better tumor recognition by lymphocytes after BRAF or combined BRAF and MEK inhibition through several mechanisms such as tumor antigens release following tumor cell death, increased expression of melanocyte differentiation antigens, increased tumor T-cell infiltration and cytotoxic activity, and decreased immunosuppressive cytokines in the tumor’s microenvironment [12,13,14,15,16,17,18,19,20,21]. The gene discussed is BRAF; the disease is neoplasm.