Moreover, pretreatment with omentin negatively modulated the TNF-α dependent phosphorylation and activation of inflammatory signaling pathways such as p38 or JNK, leading to an impaired production of cytotoxic stress molecules [6–8]. In vivo, elevated omentin serum concentrations were found in patients with obesity, diabetes, inflammatory bowel diseases, rheumatoid arthritis, asthma, coronary artery disease, and heart failure. The gene discussed is ITLN1; the disease is rheumatoid arthritis.