So far, the knowledge we have on GPR26 role belong to studies from Caenorabditis elegans, where depletion of GPR26 increases fat storage, and from rodents, where GPR26 deficiency in the hypothalamus increases genetic susceptibility to the onset of obesity, including glucose intolerance, hyperinsulinemia, and dyslipidemia (61). The gene discussed is GPR26; the disease is hyperinsulinism.