CYP1A1 and chronic obstructive pulmonary disease: In this study, we observed that CS exposure resulted in a transient induction of AHR (Fig. 9a, T1 and T3), accompanied by persistent upregulation of CYP1A1 and CYP1B1. These findings are consistent with those reported in the airways of COPD patients and highlight the potential role of CYP1A and CYP1B family enzymes in CS-induced toxicity and carcinogenicity (Pierrou et al. 2007).