For instance, high levels of CXCL1 (KC) and CXCL2 (MIP-2) have been observed in a number of murine disease models: virus-infected epithelial cells release multiple chemokines that direct neutrophil chemotaxis; peptides that inhibit CCL5/CXCL4 heterodimer formation alleviate atherosclerosis in a mouse model; and the CXCL7/CXCL4 pair compared to CXCL7 alone shows differential activity for neutrophil adhesion and transendothelial migration [29,47,48,49]. Here, CCL5 is linked to atherosclerosis.