Melanoma is a highly immunogenic cancer associated with massive immune cell infiltration. The high immunogenicity of melanoma is attributed to melanoma antigens like MART-1 (melanoma antigen recognized by T cells-1), gp100, gp75 and tyrosinase (1). In spite of the heightened immune response to melanoma cell antigens, spontaneous immune-mediated regression of the disease is rare. The intractability of melanoma has often been associated with the immunosuppressive tumor milieu and the activation of immune checkpoints like CTLA-4 (cytotoxic T-lymphocyte-associated protein 4) and PD-1 (Programmed cell death 1). CTLA-4 and/or PD-1 (or its ligand, PD-L1) act as immune checkpoints by mediating reduction in the cytotoxic activity of cytotoxic T lymphocytes (CTLs) thus leading to immune exhaustion. CTLA-4 mediates T cell anergy by attenuating CD28 signaling or inducing cell cycle blockade. PD-1 on the other hand attenuates the antigen-specific signals thus inducing T cell unresponsiveness (2).