Furthermore, the percentage of DCs expressing MHC-II, CD80, and CD86, the level of mRNA expression of IL-12 and TNF-α by DCs, and the level of DC-mediated T-cell proliferation was all decreased, both in vivo and in vitro, when PINK1 was knocked out, suggesting that PINK1 knockout prevented the function of DCs during sepsis. The gene discussed is CD86; the disease is Sepsis.