The slow PLR appeared to be independent of the structure and topography of the outer retina and included patients with retina-wide (GUCY2D), macular (CEP290 and NPHP5) or foveal (RPGRIP1) retention, as well as those with retina-wide degeneration (AIPL1-associated LCA). This evidence concerns the gene IQCB1 and Leber congenital amaurosis.