Heterozygous loss of Rac1 in cardiomyocytes, or treatment with the Rac1 inhibitor NSC23766, limited cardiac hypertrophy and improved systolic function following transverse aortic constriction (TAC)-induced pressure overload in association with blunted mineralocorticoid receptor activation and NOX activity [6]. Here, RAC1 is linked to cardiac hypertrophy.