The etiology of RS is not well known, however, it has been suggested that RS occurs due to the partial defect or lack of OATPs, including OATP1B1 and OATP1B3, which are located on the basolateral surface of hepatocytes and function to excrete organic anions, bile acids and bilirubin bile sinusoids (5,6). This evidence concerns the gene SLCO1B1 and X-linked retinoschisis.