SMAD3 and non-small cell lung carcinoma: Notably, exposing normal pulmonary fibroblasts to cigarette smoking particles condensed into culture medium was sufficient to elicit a time‐ and dose‐dependent increase in SMAD3 DNA promoter methylation, whereas such epigenetic event did not occur in its closely related homolog SMAD2, thereby providing the first rationale for the puzzling epidemiologic observation that smoking is associated with a lower risk of radiotherapy‐induced pneumonitis/fibrosis in NSCLC [92].