CCL17, a ligand of CCR4 enables Tregs recruitment to the site of infection where they induce immune suppression by TGF-β1 production; hence we investigated if CCR4 blockade could control HBsAg-specific CCL17 secretion by T cells and we found a significant reduction in CCL17 production post CCR4 blockade, which might further benefit in restricting Tregs effector function in CHB patients (Fig. 5H). The gene discussed is CCR4; the disease is infection.