A large amount of immunoparalysis of DCs (with decrease in the expression of costimulatory molecules, reduction of the release of pro‐inflammatory cytokines and increase in the release of immunosuppressive factors) developed during sepsis,3, 14 which in turn promoted the generation of Tregs, as well as inhibited the activation of NK cells, CD4+ and CD8+ T cells, causing sepsis‐associated immunosuppression.12 The gene discussed is CD4; the disease is Sepsis.