In summary, this study demonstrates that BMSCs‐Exos promote M2 polarization and suppress M1 polarization of alveolar macrophages via miR‐137‐3p mediated regulation of the TRIM24/CBP/STAT6 pathway (Figure 6 illustrates the mechanisms) suggesting their potential as a novel therapeutic strategy for ALI. Here, TRIM24 is linked to acute respiratory distress syndrome.