Furthermore, NSCLC can develop immunosuppression in the hypoxic environment through the HIF-1α/LOXL2/EMT/tumor-infiltrating lymphocytes (TILs) axis, while HIF-1α inhibition combined with anti-PD-1 therapy can repress hypoxia-induced EMT, increase CD8+ T cell infiltration, and promote antitumor immunity [78]. The gene discussed is HIF1A; the disease is non-small cell lung carcinoma.