Recent evidence demonstrates that B7-H3-expressing NSCLC escapes antitumor immunity via CD8+ T-cell repression despite anti-PD-1 immunotherapy and that B7-H3 blockade, especially in combination with the PD-1 blockade, exhibits potent antitumor efficacy mediated by increased number of tumor-specific CD8+ T cells [22]. The gene discussed is CD8A; the disease is neoplasm.