Among them, 55 individuals (49 families) with non-syndromic LCA or EOSRD carried recessive variants in CRB1, CEP290, GUCY2D, LCA5, NMNAT1, RDH12, RPGRIP1, SPATA7, or TULP1 or a dominant variant in CRX. This evidence concerns the gene LCA5 and Leber congenital amaurosis.