FPR2 and pulmonary fibrosis: AnxA1 is a 37-kDa calcium-phospholipid–binding protein highly expressed in myeloid cells and regulated by glucocorticoids.6 By interacting with its receptor, formyl peptide receptor 2/lipoxin A4 receptor (FPR2/ALX), AnxA1 down-regulates the production of proinflammatory mediators, such as eicosanoids, nitric oxide, and interleukin (IL)-6, reduces neutrophil migration to inflammatory sites, and promotes the clearance of apoptotic granulocytes.6,7 Furthermore, recent works suggest that endogenous AnxA1 may orchestrate epithelial repair8,9 and even counteract the development of lung fibrosis.10