A specific role for OX2R in promoting energy expenditure is supported by evidence that this resistance to dietary obesity is found in OX overexpressors lacking OX1R but not in those lacking OX2R and that chronic ICV injection of [Ala11, D-Leu15] OX-B, which binds to OX2R, prevents the development of fat-induced obesity [37]. The gene discussed is HCRTR1; the disease is obesity disorder.