The associations between mutations in STRA6 and incidence of Matthew-Wood syndrome have been used to create animal models for Matthew-Wood Syndrome in later research, such as with the work of the von Lintig lab in 2008, where they found that excess holo-RBP4 in circulation disrupts vitamin A uptake and causes developmental abnormalities, such as those seen in Matthew-Wood Syndrome, using a morpholino approach to generate a Stra6-deficient zebrafish model [35]. The gene discussed is RBP4; the disease is Matthew-Wood syndrome.