These chemically induced models alter multiple genes and pathways (PI3K-Akt, TNF, JAK-STAT, MAPK, Chemokine, NF-kappa B, TGF-beta signaling pathways, Apoptosis, and Cell cycle) and result in the development of hepatitis [13], which may be similar to that of HBV-induced hepatitis. This evidence concerns the gene AKT1 and hepatitis A virus infection.