In summary, PKC-θ−/− mice are resistant to ConA-induced hepatitis, and this resistance is due to at least following mechanisms: 1) reduced NKT cell number due to an intrinsic requirement of PKC-θ for NKT cell development, and 2) reduced levels of inflammatory cytokines such as IFNγ and IL-4, because PKC-θ mediates the critical signals required for NKT activation. This evidence concerns the gene PRRT2 and hepatitis A virus infection.