Cardiomyocyte-specific Rac1cKI mice did not develop cardiac hypertrophy in the absence of stimulus (Figure 2C) and had no significant changes in cardiac structure or function compared with control genotypes as assessed by echocardiography up to 4 months of age (Figure 2, D–H, and Supplemental Table 1), suggesting modification of Rac1 at Cys-178 is largely dispensable for basal cardiac function. Here, RAC1 is linked to cardiac hypertrophy.