FOXA2 and hydrops fetalis: Pathway analyses revealed transcriptional mechanisms restituted by NAD+, with significant enrichment of NFkB, HIF1 and HNF3 transcriptional networks (Fig. 4d); and de novo motif discovery in the promoters of genes whose expression appeared dysregulated only in the HF group identified strong similarities to NFkB-p65/RELA and FOXA1/FOXA2 (HNFα/HNF3β) binding sites (Fig. 4e).