However, the use of β2-m−/− mice and cells as models for Class Ia deficiency is complicated by the fact that β2-m is also an important accessory molecule for the cell surface expression of multiple non-classical major histocompatibility complex (MHC) Class Ib molecules, including CD1d, M3, FcRn, Qa-1, and HFE (reviewed in [45,46]). This evidence concerns the gene B2M and hyperinsulinemic hypoglycemia, familial, 4.