Neutrophil migration through vessels involves several stages of interactions with endothelium: tethering-rolling, stable adhesion, and diapedesis. Annexin 1 (ANXA1) and its N-terminal peptide (Ac2-26) directly interact with 2 G-protein-coupled receptors (FPR and ALX/FPRL1) to halt neutrophil diapedesis. Glucocorticoid-stimulated proteins (ANXA1 and Ac2-26), as well as aspirin-triggered lipoxin A₄ (ATL), converge at the same receptor ALX/FPRL1 to both control excessive neutrophil infiltration and limit inflammatory responses. Illustration by Marie Dauenheimer.