In a well-established mouse model for MS, the experimental autoimmune encephalomyelitis (EAE), the authors observed that animals having a myeloid-specific HO-1 deficiency showed persistent activation of antigen-presenting cells (APCs), enhanced Th17 infiltration, and increased myelin-specific T cell reactivity resulting in a higher disease activity (Tzima et al., 2009). This evidence concerns the gene HMOX1 and myeloid sarcoma.