This is showing which miR-23b can be an appropriate target for treatment of MS through IL-17 reduction, suppressed tumor necrosis factor alpha (TNF-α)- or IL-1beta-induced nuclear factor kappa-B (NF-κB) activation, and inhibit TGF-β-activated kinase 1/MAP3K7 binding protein 2 (TAB2), TAB3, and NF-κB kinase subunit alpha (IKK-α) in EAE mice (Zhu et al. 2012). This evidence concerns the gene IL17A and myeloid sarcoma.