Our cellular studies have indicated that IH, a hallmark manifestation of SAS, is involved in the reduction in glucose-induced insulin secretion by down-regulation of CD38 in pancreatic β cells [6]; the up-regulation of selenoprotein P and HIP/PAP via down-regulation of miR-203 in hepatocytes [5]; the up-regulation of adipokines, such as CCL2, TNF-α, and RETN via down-regulation of miR-452 in adipocytes [78]; and the up-regulation of myokines, such as IL-8, osteonectin, and myonectin, in myocytes [79,80,81], all of which can contribute to obesity [82]. The gene discussed is RETN; the disease is obesity disorder.