STAT3 and chronic obstructive pulmonary disease: We previously demonstrated that the mechanism of BYF against COPD might involve reducing inflammatory cytokines and oxidative stress, regulating immune response and lipid metabolism [12–15], restoring the Th17/Treg balance by activating adenosine 2a receptor [16], modulating the activities of STAT3 and STAT5 in COPD rats [17], and suppressing interleukin expression and/or secretion [18].