For instance: (i) it is expressed in macrophages in human atherosclerotic lesions, where it accelerates atherosclerosis development through effects on bone marrow-derived cells [101]; (ii) FPR2 expression in the carotid artery is associated with clinical signs of cerebral ischemia and a more stable atherosclerosis plaque phenotype [101]; (iii) FPR2 expression in smooth muscle cells (SMC) is coupled to increased collagen production and maturation, and to pathways of decreased collagen degradation [101]. The gene discussed is FPR2; the disease is brain ischemia.