These data suggest TCR stimulation by a high affinity tumor antigen, such as p15E, would generate similarly functional anti-tumor efficacy in WT vs. ALK5ΔCD8 animals (i.e., at maximum threshold); while lower affinity p15E-negative CD8+ effector T cells may be the population that is enriched following TGFβ blockade, and responsible for the improvement in anti-tumor efficacy observed. The gene discussed is CD8A; the disease is neoplasm.