We demonstrated that β-catenin suppression directly increases IFN signaling molecules and antigen presentation machinery components in β-catenin-mutated HCC murine models, with forced expression of either IRF2 or POU2F1 in two β-catenin-mutated HCC models sufficient to delay tumor development and convert a non-T cell-inflamed to a T cell-inflamed tumor. The gene discussed is POU2F1; the disease is neoplasm.