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When tissue folate and cobalamin stores are intact, an abnormal increment of postmethionine-load homocysteinemia may also reveal a saturation of the transsulfuration pathway caused by dietary methionine excess that might be combined with transsulfuration defects (in cases with basal hyperhomocysteinemia) or with the homozygous thermolabile MTHFR defect (in cases with normal fasting homocysteine) (Cattaneo, 1999)

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Notably, QMP engineering ensures favorable pH-dependent FcRn binding, also in the absence of the C-terminal leucine residue