Increased FABP4 in pulmonary epithelial and endothelial cells drives immunopathology in various models of airway inflammation, and its inhibition or genetic deletion reduces proinflammatory cytokines, immune cell recruitment, and improves airway function (Shum et al, 2006; Ghelfi et al, 2013; Wang et al, 2017). The gene discussed is FABP4; the disease is inflammatory response.