In an experimental autoimmune encephalitis (EAE) model of MS [165], knockdown of AhR exacerbated disease severity, whereas activation of AhR using agonists, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), I3C, and DIM suppressed EAE progression. The gene discussed is AHR; the disease is myeloid sarcoma.