After 8 weeks of pressure overload, we observed increased cardiac hypertrophy (Figure 4, A and B), pulmonary edema (Figure 4C), and interstitial cardiac fibrosis (Figure 4, A and D) in TAC-operated Rac1cKI mice compared with TAC-operated control mice, indicating more severe cardiac disease and heart failure in the absence of Rac1 S-palmitoylation in response to long-term pressure overload. This evidence concerns the gene RAC1 and cardiac hypertrophy.