Defects in genes such as EctodysplasinA1 (EdaA1) (tumor necrosis factor [TNF] ligand; Tabby), Edar (TNF receptor; Downless), and Edaradd (death domain adaptor; Crinkled) lead to severely abnormal cusps and molar teeth in mice and hypohidrotic ectodermal dysplasia (HED) in human [20–25]. This evidence concerns the gene EDA and hypohidrotic ectodermal dysplasia.