Postnatal treatment was partially effective in animal models but not in human patients [13], whereas prenatal administration of a recombinant EDA1 molecule, Fc-EDA, to affected boys resulted in normal sweat gland endowment and sweating ability, development of more teeth, and normalized function of salivary glands [13,14] and, thus, showed the potential to permanently resolve the most relevant clinical problems associated with XLHED [15]. This evidence concerns the gene EDA and X-linked hypohidrotic ectodermal dysplasia.