In COPD mouse models, intranasal administration of anti-miR-195 lentiviruses or miR-181c mimics attenuates neutrophil and macrophage infiltration, lung parenchymal destruction, and levels of proinflammatory factors in bronchoalveolar lavage fluid (BALF),[28] while intranasal delivery of short hairpin RNA (shRNA) lentivirus against TUG1 blocks cigarette smoking (CS)-induced inflammation and remodeling.[29] CS-induced increases in neutrophils, macrophages, and BALF cells could also be significantly reduced with lentivirus-based knockdown of circRNA forkhead box O3 (circFOXO3) in vivo. The gene discussed is TUG1; the disease is chronic obstructive pulmonary disease.