N6 methyladenosine (m6A) is a very rich mRNA modifier, which plays animportant role in biological processes such as lipid metabolism, autophagy,macrophage activity and inflammatory response.However, the role of m6A regulatorin COPD remains unknown.In this study, the expression values of 23 m6Amethylation regulators were obtained by analyzing the gene expression matrix ofCOPD patients and normal controls in GSE76925 data set.Eleven candidate m6Aregulators were selected by random forest model to construct nomination graphmodel and predict the risk of COPD.The decision curve found that patients couldbenefit from the nomination model constructed.By consensus cluster analysis, m6Aregulators in COPD patients were divided into two subtypes (clusterA andclusterB) .The m6A pattern was quantified by principal component analysis algorithm.It was found that the m6A score of patients in clusterA was higher than that ofclusterB.Differential genes (DEGs) were screened by m6A typing and the differentialgenes were analyzed by Kyoto genome and genome Encyclopedia (KEGG). It wasfound that the differential genes were mainly enriched in NF-kB and TNF signalpathway.In addition, through gene and immune cell correlation analysis, it was foundthat the patients in m6A clusterB were related to the immunity dominated byneutrophil and eosinophil traps,however the patients in clusterA are related to theimmunity dominated by monocyte traps.Therefore, the discovery of m6A patternthrough m6A typing related genes and immune cells may be a new strategy to guidethe treatment of COPD.