Mutations in the MAT1A gene are reported to cause MAT I/III deficiency, a condition characterized by persistent hypermethioninemia not accompanied by elevated homocysteine or tyrosine.36 Disturbance in the methionine cycle has been found to cause NTDs in experimental models in the mouse.31 However, clinical manifestations of MAT deficiency are variable, including no neurological abnormalities.36 Also, a stop‐gain variant c.1893C>A (p.Tyr631Ter) was detected in the nitric oxide synthase 2 (NOS2) gene (Figure 2C). The gene discussed is MAT1A; the disease is disorder of methionine catabolism.