ALG6 and hyperinsulinemic hypoglycemia, familial, 4: In opposition to this view, mammalian cell line models of ALG6 homolog deficiency (α-1,3 glucosyltranferase) and MPDU1 deficiency have demonstrated that immature LLOs (Man5GlcNAc2 and Man9GlcNAc2) can be transferred to substrate proteins at reduced rates [46], [47] and that NLG is therefore not a simple serial process where loss of one enzymatic step completely incapacitates the glycosylation machinery.