While PKCε actvation has been linked with cardioprotection in setting of acute ischemic/reperfusion injury (Inagaki et al., 2006), activation of PKCε in chronic settings is detrimental and pharmacological inhibition of PKCε attenuated cardiac fibrosis and cardia dysfunction in a rat model of HF (Inagaki et al., 2008). Here, PRKCE is linked to fibrosis.