Using cell type–specific disruption of Clcn2 we now show that the lack of ClC-2 in Sertoli cells, but not germ cells, recapitulates the testicular phenotype of Clcn2−/− mice and that Clcn2 disruption in RPE cells is sufficient to explain their retinal degeneration. This evidence concerns the gene CLCN2 and retinal degeneration.