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There is increasing evidence that pulmonary inflammation contributes to the pathogenesis of chronic lung disease (CLD).1 Cytokines are key factors in the inflammatory response. The response of various cytokines to stressful stimuli have been shown to be partly due to interindividual variation at a genetic level.2 The possibility that genetic factors play a role in susceptibility to CLD has been reported.3,4 We decided to investigate whether gene polymorphisms for tumour necrosis factor α (TNFα-308 G/A) and interleukin …