Furthermore, to determine whether long-term suppression of LHLepr → vlPAG neuronal activity rescues the tendency of ELT mice to develop HFD-induced obesity, we injected HSV-DIO-Flp into the vlPAG and AAV expressing the Flp-dependent Kir2.1 potassium channel (AAV-fDIO-eGFP-Kir2.1)46 into the LH of ELT Lepr-Cre mice, thereby inducing chronic hyperpolarization in the LHLepr → vlPAG neurons (Fig. 5i). The gene discussed is KCNJ2; the disease is obesity disorder.