We have previously reported that overexpression of CXCR4 successfully prevented hypertrophy in trans-aortic constriction (TAC)-challenged mice [21] and that isoproterenol challenge in CXCR4 deficient mice resulted in cardiac hypertrophy [22]; these findings, in conjunction with the data presented in our current study suggest a powerful regulatory role for the CXCR4/CXCL12 axis. This evidence concerns the gene CXCL12 and cardiac hypertrophy.