Therefore, the rationale behind the development of immune checkpoint inhibitors (ICIs) as anticancer therapy is to trigger the activation of immune checkpoint pathways, such as programmed cell death protein 1 (PD-1) and its ligand (PD-L1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), allowing the host’s immune system to mount an effective T-cell-mediated immune response against tumor cells [3]. Here, CTLA4 is linked to neoplasm.