Consequently, immune checkpoint blockade has managed to benefit many melanoma patients, presumably due to the activation of dormant/suppressed TSA-specific CTL, through the abrogation of PD-1:PD-L1 interactions in the TME (by anti-PD-1/PD-L1) [98,99] and possibly through the suppression of Treg function (by anti-CTLA-4) in the TME or draining lymph nodes [100,101]. Here, CTLA4 is linked to melanoma.