Although hepatic RORγt+ ILCs produce IFN-γ which is one of the pathological factors in CCl4-induced hepatitis, [24] that function of hepatic RORγt+ ILCs seems to be not critical for the development of hepatitis since there was no difference between the livers from CCl4-administrated RAG-2−/− mice and RAG-2−/− × RORγt−/− mice in terms of the expression of IFN-γ. The gene discussed is IFNG; the disease is hepatitis A virus infection.