C1QTNF3 (C1q and TNF-related protein 3, also termed CTRP3) is a secreted adipokine expressed across multiple tissues that plays key roles in metabolic regulation and immune homeostasis. Functionally, C1QTNF3 normalizes blood glucose through multiple mechanisms and modulates cytokine expression to reduce insulin resistance 1. The protein acts as a negative regulator of inflammatory responses, particularly by suppressing Th17 cell differentiation through the AdipoR2 receptor axis, thereby controlling autoimmune disease development 2. C1QTNF3 competes with Bufalin for PTGR2 binding to regulate NF-κB-mediated inflammation and oxidative stress in myocardial ischemia-reperfusion injury 3. In rheumatoid arthritis and experimental autoimmune encephalomyelitis models, C1qtnf3 deficiency exacerbates disease severity, indicating protective anti-inflammatory roles 4. Disease relevance spans metabolic disorders (diabetes and its complications), autoimmune conditions, and cancer—C1QTNF3 shows elevated expression in prostate cancer with diagnostic potential (AUC=0.972 in some datasets) 5 and in ovarian cancer bowel metastases 6. Recent genetic studies identified C1QTNF3 as a novel candidate gene associated with skin pigmentation and disease susceptibility 7. Additionally, C1QTNF3 emerged as a key fibroblast-associated gene with diagnostic value in osteoarthritis 8. These findings position C1QTNF3 as a multifunctional adipokine with therapeutic potential for metabolic, inflammatory, and autoimmune disorders.