Antibody-mediated neutralization of ICAM-1 blocked myocardial macrophage accumulation and reduced fibroblast proliferation, TGF-β1 expression, and myocardial fibrosis, although arterial pressure and LV or cardiomyocyte hypertrophy did not differ from those treated with control IgG (Kuwahara et al., 2003). This evidence concerns the gene TGFB1 and Myocardial fibrosis.