Moreover, Okada et al. showed that cathepsin H deficiency impairs the TLR3-mediated activation of the interferon regulatory factor 3 (IRF3) and interferon-β (IFN-β) secretion from dendritic cells, thus enhancing Th1 cell differentiation and resulting in early-onset EAE in an animal MS model [217]. The gene discussed is IRF3; the disease is myeloid sarcoma.