These markers tend to mark exhausted T cells with reduced antitumor functions, but phenotypic identification of certain activated versus exhausted T cells remains incompletely defined.16 Together, these data strongly suggest ERβ-dependent augmentation of antitumor CD8+ T cell effector activity and improved tumor immune cell trafficking, which could be from increased dendritic cell activation and/or CD4+ T cells as immune mechanisms for ERβ-driven antitumor activity. The gene discussed is ESR2; the disease is neoplasm.