It has been reported that inhibition of CCR3 restricted the IFN-γ-medicated changes in MCP-3, MIP-5, and RANTES in neutrophils.[67] The administration of IFN, or IFN-γ, in neutrophils subsequently activated the expression of CCR3-mediated factors and CCR3 signaling, as well as the migration of neutrophils.[67] Moreover, the immunotherapies for immunosuppression including anti-PD-1/PD-L1, Recombinant IL-15, and thymosin α1 increase the production of IFNγ and decrease the secretion of IL-10 in patients, animal and cellular model of sepsis-induced immunosuppression[8,33,36–39] 7. The gene discussed is CCR3; the disease is Sepsis.