Respiratory failure due to lung damage is accompanied by airway contraction, which can be induced by various damage-associated molecular patterns, among which mitochondrial N-formyl peptides act via FPR272. AERD is another disease in which the overactivated LXA4/FPR2 pathway exacerbates the pathogenesis. Because AERD is associated with arachidonic acid metabolism, the role of FPR2 in recognizing LXA4 is important in regulating AERD progression. Single-nucleotide polymorphism analyses have been conducted in AERD patients, showing that these patients have a high frequency of homozygote of the minor allele, FPR2-4509T>G. This minor allele is correlated with higher FPR2 levels in CD14+ monocytes, and carriers show defective lung function upon aspirin challenge63.