It may reduce the inflammation of COPD by regulating the PI3K/Akt-Nrf2 pathway and control transcription factors such as NF-κB and AP-1 to inhibit the production of inflammatory cytokines.140 Animal models provided further evidence that clarithromycin has an inhibitory effect on the development of emphysema, and its dose is almost the same as the clinical dose.223 The potential benefit of a new antibiotic, solithromycin was studied for the long-term treatment of COPD, but due to the early termination of the study, there were too few subjects and data collected to perform statistical analysis. The gene discussed is NFKB1; the disease is chronic obstructive pulmonary disease.