Similar to that in AE with anti-NMDAR antibodies, the pathogenesis of AE with anti-AMPAR antibodies was proposed that in the way of increasing internalization and degradation of surface AMPAR clusters, anti-GluR1 or anti-GluR2 antibodies in patients selectively eliminated the surface amount and synaptic localization of AMPAR (100). This evidence concerns the gene GRIA1 and acrodermatitis enteropathica.