This process involves a complicated, gradient-dependent interplay, with a variety of participating biochemical pathways such as wingless and Int-1 (WNT)/β-catenin, ectodysplasin A (EDA), Sonic hedgehog (SHH), Notch, and bone morphogenetic proteins (BMPs), that result in changes in the fate of HF progenitor cells present in both cell layers of the skin. The gene discussed is EDA; the disease is hydrops fetalis.