RARRES2 encodes chemerin, a multifunctional adipokine that regulates metabolism, inflammation, and immune responses through G-protein coupled receptors including CMKLR1, CMKLR2, GPR1, and CCRL2 1. RARRES2 positively regulates adipocyte differentiation and modulates expression of genes involved in lipid and glucose metabolism [UniProt summary]. Mechanistically, chemerin activates CMKLR1 on innate immune cells (macrophages, dendritic cells, natural killer cells) to promote leukocyte chemotaxis 1, while also exerting anti-inflammatory effects by inhibiting NF-κB signaling and promoting nitric oxide production in endothelial cells. RARRES2 exhibits context-dependent roles in disease: downregulation promotes brain metastasis in triple-negative breast cancer through lipid metabolic reprogramming via the PTEN-mTOR-SREBP1 pathway 2, while genetic variants associate with increased diabetic kidney disease risk and elevated serum chemerin levels 3. RARRES2 expression is altered in intervertebral disc degeneration 4, suggesting involvement in degenerative joint disease. Clinically, chemerin's dual pro- and anti-inflammatory properties link chr7 inflammation to obesity-related disorders including type 2 diabetes and cardiovascular disease 5. However, RARRES2 polymorphisms showed no significant independent association with acute myocardial infarction after adjusting for standard risk factors in one Iranian cohort 6, indicating context-dependent disease relevance.