It is conceivable that enhanced local production and LSEC-mediated transport and presentation of the CXCR3 ligands supported hepatic recruitment of CXCR3+ effector CD4+ T cells triggering inflammation as well as CXCR3+ regulatory CD4+ T cells necessary to suppress hepatitis [58] and the balance of the cells recruited will determine the outcome of the liver disease. The gene discussed is CXCR3; the disease is hepatitis A virus infection.