To investigate the role of Rac1 S-palmitoylation in cardiomyocytes in response to another chronic model of cardiac hypertrophy induced by left ventricular overload and mechanical stress, we subjected 8- to 10-week-old Rac1cKI mice to TAC, followed by assessment of cardiac functional and structural changes by echocardiography, histopathology, and molecular analyses. This evidence concerns the gene RAC1 and cardiac hypertrophy.