GJB2 and KID syndrome: 1998)) causes profound deafness but does not result in the devastating pathologies characteristic of KID syndrome in either human or rodent models (Sun et al. 2009; Wang et al. 2009). This has led to the suggestion that the syndromic pathologies arise from a gain of function caused by the KID syndrome mutations. One common suggestion is that the Cx26 hemichannels carrying the KID syndrome mutations are leaky, and thus cause cell death (Gerido et al. 2007; Mhaske et al. 2013).