A previous study suggests that excessive activation of TLR2/4/7 drove airway inflammation in COPD by enhancing the nuclear export of TLR2 mediated by exportin XPO6 in monocytes, which leads to increased production of TNF-α and IL-6 through the activation of TLR2/MyD88/NF-κB pathway (169). This evidence concerns the gene NFKB1 and chronic obstructive pulmonary disease.