Finally, Göser et al. [135] found that the same chemokines CCL2 and CCL3, acting through their receptors CCR2 and CCR5, are key chemokines for the development of experimental autoimmune myocarditis and proved that inhibition of CCL2 with 7ND gene transfection significantly reduced disease severity in an experimental model of autoimmune myocarditis. The gene discussed is CCL3; the disease is autoimmune myocarditis.