In contrast to the cellular responses raised against most viral infections in which CD8+ T cells play a predominant role, the resolution of HAV seems to rely on CD4+ T cells that act early in infection and produce numerous cytokines, including IFN-γ, TNF-α, IL-2 and IL-21.42 Our research group has reported that HAV-infected children show overexpression of TNF-α, IL-1, IL-6, IL-13 and monocyte chemoattractant protein-2 (MCP-2), all of which correlate with high serum levels of CBR (>2 mg dl−1). The gene discussed is CD8A; the disease is viral infectious disease.