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The genetic conditions are: (1) Homocystinuria due to cystathionine \u03b2\u2010synthase (CBS) deficiency. At least 150 different mutations in the<jats:italic>CBS<\/jats:italic>gene have been identified since this deficiency was established in 1964. Hypermethioninemia is due chiefly to remethylation of the accumulated homocysteine. (2) Deficient activity of methionine adenosyltransferases I and III (MAT I\/III), the isoenzymes the catalytic subunit of which are encoded by<jats:italic>MAT1A<\/jats:italic>. Methionine accumulates because its conversion to<jats:italic>S<\/jats:italic>\u2010adenosylmethionine (AdoMet) is impaired. (3) Glycine<jats:italic>N<\/jats:italic>\u2010methyltrasferase (GNMT) deficiency. Disruption of a quantitatively major pathway for AdoMet disposal leads to AdoMet accumulation with secondary down\u2010regulation of methionine flux into AdoMet. (4)<jats:italic>S<\/jats:italic>\u2010adenosylhomocysteine (AdoHcy) hydrolase (AHCY) deficiency. Not being catabolized normally, AdoHcy accumulates and inhibits many AdoMet\u2010dependent methyltransferases, producing accumulation of AdoMet and, thereby, hypermethioninemia. (5) Citrin deficiency, found chiefly in Asian countries. Lack of this mitochondrial aspartate\u2013glutamate transporter may produce (usually transient) hypermethioninemia, the immediate cause of which remains uncertain. (6) Fumarylacetoacetate hydrolase (FAH) deficiency (tyrosinemia type I) may lead to hypermethioninemia secondary either to liver damage and\/or to accumulation of fumarylacetoacetate, an inhibitor of the high K<jats:sub>m<\/jats:sub>MAT. Additional possible genetic causes of hypermethioninemia accompanied by elevations of plasma AdoMet include mitochondrial disorders (the specificity and frequency of which remain to be elucidated). Non\u2010genetic conditions include: (a) Liver disease, which may cause hypermethioninemia, mild, or severe. (b) Low\u2010birth\u2010weight and\/or prematurity which may cause transient hypermethioninemia. (c) Ingestion of relatively large amounts of methionine which, even in full\u2010term, normal\u2010birth\u2010weight babies may cause hypermethioninemia. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ajmg.c.30293","type":"journal-article","created":{"date-parts":[[2011,2,9]],"date-time":"2011-02-09T21:28:43Z","timestamp":1297286923000},"page":"3-32","source":"Crossref","is-referenced-by-count":167,"title":["Hypermethioninemias of genetic and non\u2010genetic origin: A review"],"prefix":"10.1002","volume":"157","author":[{"given":"S. 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