Molecular analysis in our families identified three new pathogenic variants: novel homozygous deletion c.3113_3114delCT identified in RPGRIP1. The second missense pathogenic variant p.V887G is localized in GUCY2D, gene, estimated to account for 20% of LCA cases20 and constitute the most common cause of the disease. Here, RPGRIP1 is linked to Leber congenital amaurosis.