Echocardiography analyses revealed more severe left ventricular dilation and systolic dysfunction in Rac1cKI mice with transgenic AT1R expression as early as 2 months that continues to progress at 4 and 6 months of age, highlighting a significantly more severe dilated cardiomyopathy phenotype in Rac1cKI mice with transgenic AT1R expression compared with mice with AT1R overexpression on its own (Figure 5, E–H, and Supplemental Tables 4–6). Here, AGTR1 is linked to dilated cardiomyopathy.