These pathways include the cell–cell junction reconstruction [38], increased nuclear factor-κB (NF-κB) transcription factor activity [39], activation of the transforming growth factor β (TGF-β)/fibroblast growth factor (FGF) axis coordinating the endothelial cell plasticity and smooth muscle cell migration motility [40], activation of the Smad2/3-Snail signaling pathway to increase EndMT protein expression [41], and the regulation of microRNA (miRNA) expression for a positive or negative mediation of HF progression [42]. The gene discussed is SMAD2; the disease is hydrops fetalis.