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. This evidence concerns the gene FPR2 and chronic obstructive pulmonary disease.