The liver injury induced by LPS/D-Gal in mice largely depends on the production of the pro-inflammatory and pro-apoptotic cytokine TNF-α, which usually reaches its peak level 1.5 h after LPS exposure.29 Then, the high level of TNF-α induces massive apoptosis of hepatocytes via the death receptor-dependent pathway.30 Therefore, both inhibition of TNF-α production at the early stage and suppression of TNF-α-mediated pro-apoptotic signaling at the late stage might be rational strategies for the prevention of LPS/D-Gal-induced hepatitis. The gene discussed is TNF; the disease is hepatitis A virus infection.