Furthermore, as ERAP1 is not known to function in the processing of antigens for MHC II presentation, the role of ERAP1 in MS susceptibility may be a result of its alternative cellular functions such as cytokine receptor shedding and mediating cytokine production, with TNFR1 highlighted as a susceptibility locus for MS [86]. This evidence concerns the gene TNFRSF1A and myeloid sarcoma.