Hmox1 deficient mice had increased levels of pro-inflammatory cytokines and a hyperinflammatory response to LPS exposure (83), and conditional deletion of Hmox1 in myeloid cells resulted in an exacerbated inflammatory phenotype in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis, which is dependent on activation of interferon beta signaling (84). This evidence concerns the gene HMOX1 and experimental autoimmune encephalomyelitis.