Recently, studies in melanoma have focused on combining targeted therapies such as BRAF and MEK inhibitors with ICIs, aiming to increase efficacy by tackling resistance; the biology behind this strategy is to promote immune changes within the TME, particularly the release of cancer cell antigens and antigen-presentation by APCs to T cells in a context of checkpoint inhibition, which in turn lead to the activation of effector, tumor-specific T cell clones (Chen and Mellman, 2013). This evidence concerns the gene BRAF and neoplasm.