Results showed that apolipoproteins involved in HDL metabolism (Fig. 2a, b), including structural apolipoproteins (ApoA-I and ApoE) and proteins conferring non-canonical functions to HDL, such as inhibition of inflammation, oxidative stress and retinol transport (ApoA-IV, ApoM, and RBP) were upregulated in KO-NTD embryos. The gene discussed is APOA1; the disease is neural tube defect.