For instance, in regulatory T cells (Tregs) of RRMS patients, De Santis et al. [21] showed specific upregulation of miR-106b and miR-25 which have been described to modulate TGFβ signaling through their action on p21, a potent cyclin kinase inhibitor, and BIM, a Bcl-2 homology domain, proapoptotic member of the Bcl-2 family. This evidence concerns the gene BCL2 and relapsing-remitting multiple sclerosis.