However, a causative role for ADAM22 and ADAM23 in ADLTE has been questioned in genetic studies of families without LGI1 mutations: direct sequencing of ADAM22 exons revealed no disease-causing mutations [34,35], and linkage analysis with microsatellite markers within or near the ADAM23 gene failed to reveal any significant linkage peak [36]. This evidence concerns the gene ADAM23 and autosomal dominant epilepsy with auditory features.