Further analysis of the functional pathways enriched by m6A methylation typing (DEGs) and the interaction between different methylation types and the HDAC protein revealed that the m6A methylation regulator, METTL3, might enhance the inflammatory response, airway remodelling, and airway resistance in COPD through regulatory mechanisms involving NF‐kB and HDAC protein expression. The gene discussed is METTL3; the disease is chronic obstructive pulmonary disease.