Moreover, in CL-treated animals, we did not observe any increase in TNFα mRNA levels (Figure 3D), nor did these mice develop hepatitis with increased plasma ALT levels (Figure 3E), indicating that Kupffer cells producing increased levels of TNFα were the primary cause of augmented liver damage after GalN/LPS in Pio-fed mice. The gene discussed is TNF; the disease is hepatitis A virus infection.