In asthma complicated by respiratory infection, exposure to fatty acids increases LDHA expression and lactate production in macrophages, which in turn drives excessive secretion of TNF-α, IL-6, IL-1β and NO; 2 DG abolishes these pro-inflammatory effects in both animal models and patient-derived macrophages (Xuan et al., 2024). The gene discussed is IL1B; the disease is asthma.