Since Connexin26 and Connexin 30 are co-assembled to form hybrid gap junctions and a previous mouse experiment suggested that up-regulation of Connexin or the slowing of its degradation might be a therapeutic strategy to prevent and treat deafness caused by Connexin 30 mutations (Ahmad et al., 2007), we hypothesised that for some of the patients with a more minor phenotype than other patients with the GJB2 c.235delC mutation, it is the overexpression of Connexin30 that plays a compensatory role. The gene discussed is GJB6; the disease is deafness.