However, CXCR2-dependent promotion of type 2 inflammations and accumulation of key inflammatory players such as neutrophils and eosinophils were attenuated in a mouse model of asthma exacerbation by silencing CXCL3 or CXCL5 via RNA interference, resulting in a reduction in airway hyperreactivity and mucus hypersecretion in asthmatic animals [54]. The gene discussed is CXCL5; the disease is asthma.