On the other hand, the density of CD103+CD8+ TRMs increased during anti-PD-1 treatment of responsive patients with lung cancer, with the bursting proliferative activity and cytotoxicity (e.g., granzyme B), oligoclonal expansion of the TCR-β profile clonotype and upregulated expression of Aiolos, phosphorylated STAT-3 and IL-17, which were key regulators of T helper 17 cell differentiation (61). The gene discussed is CD8A; the disease is lung cancer.