Using knockout mouse models as genetic tools, the Levine lab also described that homozygous knockout of BECN2 in mice is embryonic lethal, and monoallelic loss of BECN2 results in metabolic dysregulation (including elevated food intake, obesity and insulin resistance) partially due to increased levels of a brain GPCR cannabinoid 1 receptor. The gene discussed is BECN2; the disease is obesity due to melanocortin 4 receptor deficiency.