It has been reported that A2AR participated in regulating the NLRP3 inflammasome in macrophages and endothelial cells,15, 16 which contributed to better outcomes of bronchopulmonary dysplasia and stroke, and A2AR blockade could inhibit NLRP3 inflammasome activation and promote M2 like microglia polarization in the model of hypoxic–ischemic white‐matter damage.17 This evidence concerns the gene NLRP3 and bronchopulmonary dysplasia.