This finding contrasts with the upregulation of CXCL12 and CXCR4, respectively in the plasma and left ventricles, in patients with chronic heart failure due to coronary artery disease or dilated cardiomyopathy and in two mouse models of cardiac hypertrophy, one due to transaortic constriction and the other using transgenic RacET mice with cardiac overexpression of the small GTPase Rac1 [32]. Here, RAC1 is linked to coronary artery disorder.