The rationale behind dual CTLA-4/PD-1 blockade is evident from the differential and non-redundant immune-biologic role of the two pathways within the cancer immunity cycle, where CTLA-4 is a prominent driver of immune-suppression in tumour-antigen presenting cells and T-regs, whereas PD-1/PD-L1 predominantly downregulates the effectiveness of the CD8 + CTL response. The gene discussed is CTLA4; the disease is neoplasm.