Cardiomyocyte-specific Rac1 knockout mice were protected from streptozotocin-induced cardiac hypertrophy and fibrosis and defects in cardiac contraction and relaxation while administration of the Rac1 inhibitor, NSC23766, reduced superoxide production and apoptosis observed in diabetic db/db mice, however this did not affect cardiac hemodynamics [42]. This evidence concerns the gene RAC1 and cardiac hypertrophy.