Panel-based analysis of coding sequences and intron–exon boundaries of genes involved in LCA and differential diagnoses in 722 probands revealed biallelic RPGRIP1 pathologic variants in 26/722 individuals and single presumably loss-of-function RPGRIP1 variants (one nonsense, one 1-bp duplication, one 1-bp deletion and three consensus splice-site pathologic variants; Table 1) in 6/722 of them. This evidence concerns the gene RPGRIP1 and Leber congenital amaurosis.