Sustained increased reactive oxygen species (ROS) contributes to both airway and systemic inflammation, which are key pathological features in the development of COPD.3, 4 The overproduction of ROS, along with sustained activation of endogenous enzymes, resulted in direct damage to lung tissues exposed to CS.5, 6 Nuclear factor erythroid 2-related factor 2 (Nrf2) is a pivotal transcription factor involved in the cellular antioxidant response, while Kelch-like ECH-associated protein 1 (Keap1) binds to Nrf2 and promotes its degradation under basal conditions.7 The gene discussed is NFE2L2; the disease is chronic obstructive pulmonary disease.