Genetic studies and in vitro observations have shown potential associations of CCND1 and CCND2 with asthma and COPD.43–45 In addition, CASP3 was reported to play a functional role in airway epithelial apoptosis46,47 and pro-inflammatory cytokines (FOXO4) may contribute to regulation of muscle atrophy and smooth muscle cell migration.48,49 Altogether, miRNA-mediated airway epithelial apoptosis and pro-inflammatory cytokine pathways (hsa-let-7a and hsa-let-7b) may offer potential mechanisms for the overlapping syndrome between asthma and COPD. This evidence concerns the gene FOXO4 and asthma.