Therefore, it tends to promote the immunoregulatory pathways necessary to halt liver damage, which also explains its strong association with the transcription profiles of peripheral Cldn1and TGF-β. In another context, the inverse correlation observed in non-cirrhotic patients between sCD163 and both interleukins 10 and 12, as well as between peripheral Cldn1 and TGF-β transcription, was not surprising, considering that sCD163 mainly promotes liver cirrhosis by activating hepatic Kupffer cells that consequently overexpress IL-10 [47]. The gene discussed is CLDN1; the disease is cirrhosis of liver.