in subjects with current study showed significant difference in 25-Hydroxyvitamin D3 levels between subjects with GS and control subjects, a finding that has not been previously reported. Although the sample size in the current study may not be sufficient to make conclusions, the differences in vitamin D3 levels may be explained by defective glucuronidation in GS subjects. 25OHD3, the major circulating form of vitamin D3 in humans, blood concentration represent a balance between it’s formation and clearance by several processes. Thus, differences in the efficiency of any of these processes, including glucuronidation, may affect circulating plasma concentration of 25OHD3. Some studies identified different glucuronide conjugates of 25OHD3 and showed some variants of UGT1A that acted as principal catalysts of 25OHD3 glucuronidation in human liver . It is not clear if UGT1A defects may result in vitamin D3 alterations in subjects with GS and if Vitamin D screening is recommended in these subjects.