Considering that the results of the present study as well as the literature data indicate the main influence of TNF-α and IFN-γ on liver damage in ConA-induced hepatitis, it can be concluded that GRMS-55 exhibits a hepatoprotective activity primarily by inhibiting the production of TNF-α and, to a lesser extent, by decreasing IFN-γ signaling. This evidence concerns the gene TNF and hepatitis A virus infection.