Lipoxin A4 (LXA4) evokes mobilization of AnxA1 and acts in concert with AnxA1 through formyl-peptide receptor 2 (FPR2, which also binds LXA4, hence termed as ALX/FPR2) (60) to dampen neutrophil recruitment into inflamed tissues as shown in ischemic mesenteric postcapillary venules (59) and atherosclerotic lesions (61, 62). This evidence concerns the gene ANXA1 and Atherosclerotic lesion.