Moreover, Sutton et al. used a mouse model of experimental autoimmune encephalomyelitis (EAE), an animal model of MS, and found that Bmal1 regulated the accumulation and activation of immune cells in EAE, and the loss of myeloid Bmal1 exacerbated inflammation in the CNS through the expansion of IL‐1β secreting monocytes, which increased pathogenic IL‐17+/IFN‐γ+ T cells [107]. This evidence concerns the gene BMAL1 and myeloid sarcoma.