The delay in the development of overt cardiomyopathy in the conditional Rpsa-knockout mice may be due to decreased efficiency of the troponin T–driven CRE-expressing AAVs compared with the germline β-actin–driven CRE or due to the added effect of Rpsa deletion in noncardiomyocytes in the unconditional Rpsa-knockout mice. Here, ACTB is linked to cardiomyopathy.