We have previously shown that an up-regulation of extracellular Gal-9 presented by HCV-infected hepatocytes interacting with Tim-3 highly expressed on M/MØ (an example of ligand/receptor trans association in the setting of pathogen infection) leads to decreased IL-12 and increased IL-23 productions by inhibiting STAT-1 and/or activating STAT-3 phosphorylation [29,30]. Here, IL23A is linked to infection.