These strategies were developed to block the binding of cluster of differentiation (CD) 86 on antigen presenting cells (APC) and PD-L1 on tumour cells to the inhibitory receptors CTLA-4 and programmed death receptor-1 (PD-1) on T cells (respectively), sustaining the tumoricidal activity of cytotoxic effector T cells upon interaction with tumour cells [27]. The gene discussed is CD274; the disease is neoplasm.