In individuals with obesity, the hypoxic state of AT results in dysregulation of the adipokines, including interferon-γ (IF-γ) by T helper 1 (Th1) lymphocytes, to promote anti-inflammatory M2 macrophage transformation to the pro-inflammatory M1 phenotype (primarily derived from EAT) recruitment and polarization. The gene discussed is IFNG; the disease is obesity due to melanocortin 4 receptor deficiency.