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Hearing loss is the most widespread sensory disorder, with an incidence of congenital genetic deafness of 1 in 1600 children. For many ethnic populations, the most prevalent form of genetic deafness is caused by recessive mutations in the gene gap junction protein, beta 2, 26 kDa ( GJB2 ), which is also known as connexin 26 ( Cx26 ). Despite this knowledge, existing treatment strategies do not completely recover speech perception. Here we used a gene delivery system to rescue hearing in a mouse model of  Gjb2  deletion. Mice lacking  Cx26  are characterized by profound deafness from birth and improper development of cochlear cells. Cochlear delivery of  Gjb2  using an adeno-associated virus significantly improved the auditory responses and development of the cochlear structure. Using gene replacement to restore hearing in a new mouse model of  Gjb2- related deafness may lead to the development of therapies for human hereditary deafness.

Perinatal Gjb2 gene transfer rescues hearing in a mouse model of hereditary deafness