Besides inducing programmed cell death of BRAFV600E mutant melanoma cells, BRAF inhibition shapes the tumor microenvironment (TME), thereby influencing tumor immunogenicity.7 8 In patients with melanoma, tumor-targeted therapy increased the expression of tumor antigens and infiltration of activated T cells,9–11 while the number of myeloid-derived suppressor cells (MDSC) decreased.12 Likewise, BRAFi-treated transplantable and autochthonous melanoma mouse models showed recruitment of activated T and natural killer (NK) cells, whereas regulatory T cells (Treg) and MDSC were decreased.13–17. This evidence concerns the gene BRAF and melanoma.