The rs7665090G variant mediated risk for PBC may be driven by excessive NF-κB signaling in hepatic stellate cells, an important cell type in the pathophysiology of PBC, that exhibit striking morphological and functional similarities to astrocytes, including expression of GFAP, regulation of the blood–tissue barrier, and NF-κB-dependent recruitment of phagocytic Kupffer cells22,23. The gene discussed is GFAP; the disease is primary biliary cholangitis.