Previous studies (12, 13) found that quitting smoking could significantly increase aryl-hydrocarbon receptor repressor methylation, inhibit aryl hydrocarbon receptor activity, inhibit the proliferation, invasion, migration, and angiogenesis of lung cancer cells, promote tumor cell apoptosis, and reduce immune escape; thus, smoking may enhance the efficacy of immunotherapy for lung cancer patients, and past and current smokers with lung cancer may have different efficacies of immunotherapy. The gene discussed is AHR; the disease is lung carcinoma.