The abnormal activity of MTR could lead to accumulation of methyl THF which could not be used in folate-dependent reactions, such as thymidylate biosynthesis which is involved in NTD pathogenesis.24 It was corroborated that the polymorphism 2756A>G on MTR gene could convert asparthione to glycine.25,26 The subjects with the genotype GG were reported to have lower level of homocysteine in plasma compared with AA and AG in previous researches.27–31. This evidence concerns the gene MTR and neural tube defect.