The wild-type (WT), SIRT2+/−, and SIRT2−/− embryos all developed normally without NTDs (Supplementary Table 2), suggesting that even though SIRT2 KO increases MARCKS acetylation, a pathogenic maternal diet might not be able to induce MARCKS phosphorylation, which is a requirement for NTD formation. The gene discussed is MARCKS; the disease is neural tube defect.