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We review the molecular basis of three related basic helix–loop–helix (bHLH) genes ( Neurog1 ,  Neurod1 , and  Atoh1 ) and upstream regulators  Eya1/Six1 ,  Sox2 ,  Pax2 ,  Gata3 ,  Fgfr2b ,  Foxg1 ,   and  Lmx1a/b  during the development of spiral ganglia, cochlear nuclei, and cochlear hair cells. Neuronal development requires early expression of  Neurog1 , followed by its downstream target  Neurod1 , which downregulates  Atoh1  expression. In contrast, hair cells and cochlear nuclei critically depend on  Atoh1  and require  Neurod1  and  Neurog1  expression for various aspects of development. Several experiments show a partial uncoupling of  Atoh1/Neurod1  (spiral ganglia and cochlea) and  Atoh1/Neurog1/Neurod1  (cochlear nuclei). In this review, we integrate the cellular and molecular mechanisms that regulate the development of auditory system and provide novel insights into the restoration of hearing loss, beyond the limited generation of lost sensory neurons and hair cells.

Neurog1, Neurod1, and Atoh1 are essential for spiral ganglia, cochlear nuclei, and cochlear hair cell development