Proposed mechanisms for altered neurodevelopment in response to maternal folate deficiency are based on preclinical data, and include altered lipid and fatty acid metabolism, increased cytokines and neuroinflammatory response, DNA methylation altering gene expression, and oxidative damage; and maternal MTHFR deficiency results in hyperhomocysteinemia. The gene discussed is MTHFR; the disease is hyperhomocysteinemia.