Like the Fam20A-cKO mice, Enam-null mice also showed AI phenotypes.25, 26, 27 Thus, the lack of proper phosphorylation in and/or the reduction of ENAM might be among the contributing factors causing the enamel defects in the Fam20A-cKO mice and in human patients with AIGFS and ERS. This evidence concerns the gene FAM20A and amelogenesis imperfecta type 1G.