Overall, the proband (patient II:1) with triallelic mutations in CRB1 and SPATA7 had a phenotype similar to the other two affected brothers’, as well as better visual acuity than that of most LCA patients with other CRB1 mutations or with mutations in other LCA genes [25], suggesting that the additional mutant allele in SPATA7 might not contribute to the disease. The gene discussed is CRB1; the disease is Leber congenital amaurosis.