For example, elevated IFNγ levels have been described to increase the immunogenicity of tumor cells, thereby triggering a tumor-directed immune response, e.g., by recruitment of lymphocytes to the TME, induction of the pro-inflammatory phenotype of macrophages, DC maturation, and differentiation of naive CD4+ T cells into Th1 effectors [44]. The gene discussed is CD4; the disease is neoplasm.