It was found that the neuron-specific ablation of LMO4 in mice results in uncontrolled activity of PTP1B, thus causing hyperglycemia, impaired leptin signaling in the hypothalamus, and obesity; conversely, the intracerebroventricular administration of trodusquemine in LMO4-deficient mice restored central leptin signaling and improved the control exerted by this hormone on blood insulin levels [90,91]. The gene discussed is PTPN1; the disease is obesity due to melanocortin 4 receptor deficiency.