PPARγ exhibits multi-target regulatory potential in respiratory diseases, particularly demonstrating significant therapeutic value in immunometabolic regulation (e.g., macrophage polarization, mitochondrial function) and airway remodeling inhibition.[12–14] Moreover, studies have clearly confirmed that PPARγ expression is lower in the airways of non-CF BIS subjects, and this low-level PPARγ expression is intrinsically linked to the presence of high levels of Pseudomonas aeruginosa.[15]. The gene discussed is PPARG; the disease is cystic fibrosis.