In hearts subjected to stress, several AKAPs involved in the maintenance of metabolic and contractile functions of cardiomyocytes, including AKAP1 (AKAP121), AKAP5 (AKAP79) and AKAP12 (gravin), are rapidly downregulated [25,26,27,28], whereas anchoring proteins promoting cardiac remodeling and heart failure, such as AKAP6 (mAKAP), are upregulated [23]. Here, AKAP5 is linked to heart failure.