Furthermore, an immune-mediated mechanism of resistance has been hypothesized; despite the initial favorable effects on the tumor microenvironment exerted by BRAFi and MEKi, low levels of CD8+ tumor-infiltrating T cells were observed in patients who rapidly progressed under targeted therapy [24], together with an increased expression of the immune inhibitory molecule programmed death-ligand PD-L1 [25]. This evidence concerns the gene CD274 and neoplasm.