In these contexts, the AR has been implicated both as a transcription factor promoting exhausted CD8+ T-cell formation and as an inhibitor of CD8+ T-cell function, activity and stemness.86, –88 Investigations into the differences in the TME of RCC between male and female patients have revealed that male RCC TME exhibits higher infiltration and exhaustion of CD8+ T cells compared to females. The gene discussed is CD8A; the disease is renal cell carcinoma.