In particular for Cx46, it has been reported that mice lacking this connexin develop cataracts due to the absence of Cx46-based communication between mature fiber cells and more peripheral cells (Gong et al., 1998) and that Cx46 mutations that result in non-functional gap junction channels (e.g., N63S and frame-shift mutant fs380) produce cataracts in human lenses (Pal et al., 2000; Berthoud and Ngezahayo, 2017; Berthoud et al., 2020). This evidence concerns the gene GJA3 and cataract.