Hence, although experimental evidence suggests that ANGPTL8 is involved in circadian liver response to food intake, glucose tolerance, insulin resistance and ectopic lipid accumulation [46–48], our results seem to imply that ANGPTL8 is not responsible for the lower levels of insulin seen in patients with PWS in comparison to controls matched for BMI SDS. This evidence concerns the gene ANGPTL8 and Prader-Willi syndrome.