Furthermore, ALX/FPR2 is activated by the anti-microbial cathelicidin LL-37, which is up-regulated in human atherosclerotic lesions (Edfeldt et al., 2006), and genetic targeting of its murine homolog, the cathelicidin-related anti-microbial peptide (CRAMP), reduces atherosclerosis burden (Doring et al., 2012). The gene discussed is CAMP; the disease is atherosclerosis.