Mutations in GJB2, the gene encoding the gap-junction protein connexin 26, are the most common cause of autosomal recessive non-syndromic deafness in many populations across the world. Recent findings show that in addition to the role in the circulation of potassium ions in the inner ear, in which other connexins are involved as well, gap junctions have been implicated in intercellular signaling among nonsensory cells, together with proteins of the epithelial support complex (ESC), and may be involved in the maintenance of the endothelial barrier in the stria vascularis.
