In addition, we have previously demonstrated that in vivo administration of synthetic peptides displacing AKAP121 from mitochondria increased cardiac ROS and apoptotic cell death, but is was not sufficient to induce cardiac hypertrophy, even if we observed increased nuclear localization of nuclear factor of activated T-cells (NFAT), the main effector of the calcineurin-dependent pro-hypertrophic signaling pathway (Perrino et al., 2010). Here, AKAP1 is linked to cardiac hypertrophy.