Notably, leptin-treated NachBac mice showed a p-STAT3 expression level comparable to that of leptin-treated ob/ob mice (Figures 3C and 3D), demonstrating that, despite severe obesity development and phenotypic leptin resistance, leptin-induced p-STAT3 signaling remains intact in Arc LepR neurons. The gene discussed is LEPR; the disease is obesity due to melanocortin 4 receptor deficiency.