Several additional immune mechanisms that may contribute to the efficacy of aHSCT in MS have include depletion of peripheral blood mucosal-associated invariant T (MAIT) cells, decrease of MS-associated inflammatory micro RNAs (miR-155, miR-142-3p, miR-16), along with increased immune T and NK regulatory cells and increased expression of immune checkpoint receptors and regulatory molecules such as PD-1, CTLA-4, GITR and TGF-b1 [127]. The gene discussed is CTLA4; the disease is myeloid sarcoma.