Auto-Abs against N-methyl-d-aspartate receptor (NMDAR) and leucine-rich glioma inactivated 1 (LGI1) proteins expressed on the neuronal surface resulting in hyperexcitability and impairment of synaptic function are considered to be pathogenic in patients with AE that is characterized by a wide range of neurological and psychiatric clinical features including cognitive impairment, behavioral changes, movement disorders and epileptic seizures (4). This evidence concerns the gene LGI1 and acrodermatitis enteropathica.