However, etoposide alone did not significantly increase the population of activated CD8+ T cells (Fig. 7g and Supplementary Fig. 7f), suggesting that etoposide-induced PD-L1 downregulation is not sufficient to reverse T cell dysfunction in the animal models and that the inhibitory effect of etoposide monotherapy on tumor burden and CSC frequency is likely attributed to the CSC-targeting cytotoxic activity of etoposide39. The gene discussed is CD8A; the disease is neoplasm.