Helicobacter hepaticus, which is more likely to colonize the colon under HBV infection, was found to act with some specific innate lymphoid cells (ILCs) to indirectly activate the IFN-γ/p-STAT1 axis, generating a detrimental immune microenvironment and accelerating the tumorigenesis of HCC (hepatocellular carcinoma) (77). The gene discussed is STAT1; the disease is hepatocellular carcinoma.