Moreover, studies of pendrin-related mouse models have revealed pathobiological mechanisms that may have broad implications beyond hearing loss associated with loss-of-function or hypo-functional mutations of SLC26A4. The concept that a temporally and spatially limited therapy may be sufficient to restore normal hearing provides an imperative to develop interventions that secure a life-time of normal hearing in children bearing mutations of SLC26A4. This evidence concerns the gene SLC26A4 and hearing loss disorder.