Being skewed toward a proinflammatory state, alterations in adipocyte-intrinsic cellular metabolism impacts adipocyte-immune cell crosstalk via changes in adiponectin, leptin, and IL-6, as well as other pro-inflammatory mediators (e.g., TNF, IL-1, type I IFNs, etc.)is dysregulated during obesity. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.