Finally, similar to the K+-recycling disruption hypothesis, our recent finding that after deletion of Cx26 in the cochlea mice can still retain normal hearing at young ages (Chen et al., 2014; Zhu et al., 2015) (Figure 4) indicates that Ca++-wave propagation impairment cannot be a principal deafness mechanism for Cx26 deficiency induced hearing loss. Here, GJB2 is linked to hearing loss disorder.