Cell surface inhibitory immune checkpoints (also known as negative costimulatory molecules), including PD-1, PD-L1, CTLA-4, TIM-3, et al, are implicated in the immunosuppression of sepsis, by functionally inhibit phagocytosis and cytokine release of immune cells and promote T-cell exhaustion (87). This evidence concerns the gene CTLA4 and Sepsis.