Indeed, myeloid-driven overexpression of human FPR2/ALX in transgenic mice resulted in a reduced neutrophil infiltration during zymosan-induced peritonitis (Devchand et al., 2003), whereas ALX/FPR2−/− mice have an exacerbated inflammatory phenotype and delayed resolution (Dufton et al., 2010). The gene discussed is FPR2; the disease is peritonitis.