Indeed, CXCR1 and CXCR2 antagonism through oral administration of Ladarixin prevented neutrophilic airway inflammation and protein leakage, peribronchial tissue remodeling, interstitial fibrosis and bronchial hyperreactivity improving pulmonary mechanics in all human disease-related models used here, including GC-sensitive and insensitive asthma, and enhanced mice survival in AECOPD model (Graphical Abstract). The gene discussed is CXCR1; the disease is asthma.