This notion was supported by the increase in Lm values, downregulation of ECM gene Ecm2 and cell adhesion molecule 2 (Cadm2), and upregulation of mucin gene Muc5ac. Our findings imply that children with persistent asthma who start smoking at a young age are at an increased risk of developing fixed airflow obstruction and COPD in adulthood, consistent with clinical observations [9]. The gene discussed is ECM2; the disease is chronic obstructive pulmonary disease.