Therefore, we speculate that F2R and Sphk1 can regulate the synthesis and/or secretion of certain interleukins in our COPD rat models, while BYF treatment does not influence transcription but reduces interleukin translation or secretion by regulating expression of F2R and Sphk1, thereby improving COPD-related inflammation (Figure 7). The gene discussed is F2R; the disease is chronic obstructive pulmonary disease.