Glucose intolerance is developed in male mice with POMC neuron-specific deficiency of leptin receptor, Lepr, (LepR) [18], autophagy-related 7, Atg7, (ATG7) [19] or Protein Kinase C λ, Prcki, (PKCλ) [20] and in female mice with POMC neuron-specific deficiency of liver kinase B1, Lkb1, (LKB1) [21] or double deletion of LepR and insulin receptor, Insr, (IR) [22], regardless of the body weight change. The gene discussed is INSR; the disease is Glucose intolerance.