Second, the cause and effect relationship between FPR1/2/3 expressions and COPD is not straight forward, but the reversal of several altered FPR expressions after 1-year treatment indicate that smoking related FPR1 over-expression and FPR2/3 under-expression could contribute to the airflow limitation in COPD, and the reversal of these imbalance could lead to the improvement in small airway dysfunction. The gene discussed is FPR1; the disease is chronic obstructive pulmonary disease.