Cochlear hair cells express SK2, a small-conductance Ca²⁺-activated K⁺ channel thought to act in concert with Ca²⁺-permeable nicotinic acetylcholine receptors (nAChRs) 9 and 10 in mediating suppressive effects of the olivocochlear efferent innervation. To probe the in vivo role of SK2 channels in hearing, we examined gene expression, cochlear function, efferent suppression and noise vulnerability in mice overexpressing SK2 channels. Cochlear thresholds, as measured by auditory brainstem responses and otoacoustic emissions were normal in overexpressers, as was overall cochlear morphology and the size, number and distribution of efferent terminals on outer hair cells. Cochlear expression levels of SK2 channels were elevated 8-fold, without striking changes in other SK channels or in the 9/10 nAChRs. Shock-evoked efferent suppression of cochlear responses was significantly enhanced in overexpresser mice, as seen previously in 9 overexpresser mice (Maison et al. 2002); however, in contrast to 9 overexpressers, SK2 overexpressers were not protected from acoustic injury. Results suggest that efferent-mediated cochlear protection is mediated by other downstream effects of ACh-mediated Ca²⁺ entry, different from those involving SK2-mediated hyperpolarization and the associated reduction in outer hair cell electromotility.