Indeed, it has been shown that homozygous offspring with targeted deletion of Cx26 in the epithelial gap junction network of the cochlea (Gjb2−/− mice) failed to acquire hearing function [79], whereas the heterozygous (Gjb2+/−) mice show an accelerated presbycusis phenotype that appears at 6 months of age [80]. The gene discussed is GJB2; the disease is presbycusis.