Our findings present a novel perspective, contrasting with prior in vivo and clinical studies that primarily focused on macrophage‐ or endothelial‐derived active ingredients as primary drivers of neutrophilic inflammation in lung diseases.[17, 18, 56, 57, 58, 59] By identifying AECs as one of the important sources of CXCL1, our work challenges the paradigm of immune cell dominance, highlighting the active and crucial involvement of structural cells in inflammatory signaling. This evidence concerns the gene CXCL1 and lung disorder.