The cell viability of LCA was also not statistically altered after knock-down of ATG7, e.g. cell viabilities were changed from 71.92% (10 μM LCA) and 53.03% (15 μM LCA) to 74.06% (10 μM LCA + siATG7) and 50.04% (15 μM LCA + siATG7), respectively (Fig. 4B). This evidence concerns the gene ATG7 and Leber congenital amaurosis.