In studies conducted by the investigators, it was found that the anti-inflammatory effect of the CAP agonist GTS-21 on DCs in sepsis-induced ALI: GTS-21 significantly inhibited the expression of MHCII, CD40, and CD86 on the surface of DCs and also the release of DC-related pro-inflammatory cytokines (IL-6, TNF-α, IL-18, IL-1β, IL-12p40, and HMGB1). The gene discussed is CD86; the disease is Sepsis.