Gong et al. [23] reported that mice homozygous for disrupted connexin 46 developed nuclear cataracts due to failure in maintenance of differentiation and of crystallins solubility, while connexin 50 knockout mice had reduced ocular growth along with nuclear cataract [24,25].Targeted replacement of connexin 50 with connexin 46 in mice has revealed the role of connexin 50 in lens and eye growth and that of connexin 46 in maintaining differentiation by nonspecific restoration of intercellular communication [26]. This evidence concerns the gene GJA8 and nuclear cataract.