CLN3 and hereditary thrombophilia due to congenital protein S deficiency: Recent experimental ocular gene therapies on animal models with soluble lysosomal enzyme deficiencies (CLN1, CLN5, CLN10, and CLN11) and transmembrane protein deficiencies (CLN3 and CLN6) have shown the strong potential of gene therapeutic approaches to effectively treat NCL-related retinopathies.