Myc family members play crucial roles in regulating cell proliferation, size, and differentiation during organogenesis. BothN-mycandc-mycare expressed throughout inner ear development. To address their function in the mouse inner ear, we generated mice with conditional deletions in eitherN-mycorc-myc. Loss ofc-mycin the inner ear causes no apparent defects, whereas inactivation ofN-mycresults in reduced growth caused by a lack of proliferation. Reciprocally, the misexpression ofN-mycin the inner ear increases proliferation. Morphogenesis of the inner ear inN-mycmouse mutants is severely disturbed, including loss of the lateral canal, fusion of the cochlea with the sacculus and utriculus, and stunted outgrowth of the cochlea. Mutant cochleas are characterized by an increased number of cells exiting the cell cycle that express the cyclin-dependent kinase inhibitor p27Kip1and lack cyclin D1, both of which control the postmitotic state of hair cells. Analysis of different molecular markers inN-mycmutant ears reveals the development of a rudimentary organ of Corti containing hair cells and the underlying supporting cells. Differentiated cells, however, fail to form the highly ordered structure characteristic for the organ of Corti but appear as rows or clusters with an excess number of hair cells. The Kölliker's organ, a transient structure neighboring the organ of Corti and a potential source of ectopic hair cells, is absent in the mutant ears. Collectively, our data suggest thatN-mycregulates growth, morphogenesis, and pattern formation during the development of the inner ear.