Our analysis enlightens several other miRNAs that previous studies have reported to be associated with MS: miR-23B, involved in MS and other autoimmune diseases by suppressing IL-17-associated inflammation that targets the proteins TAB2, TAB3 and IKK-α [78]; miR-29a/b, the deficiency of which identifies a negative feedback loop controlling Th1 bias that is dysregulated in MS [79]; and miR-27B, which is up-regulated in memory CD4(+) T cells from patients with MS, inhibiting Th2 cell development and favoring pro-inflammatory Th1 responses [80]. This evidence concerns the gene CD4 and autoimmune disease.