Inconsistent with previous reports that IL-4 is positively correlated with serum viral load and ALT to exert its suppressive effect on T helper cytokine function by promoting neutrophil survival and hepatitis [37], the observed contrasting significant correlations of IL-4 with HBeAg and HBeAb in the current study primarily demonstrates the essential regulation of Th2 cell response during HBeAg seroconversion. The gene discussed is GPT; the disease is hepatitis A virus infection.