The CaMKII-related stimulation of INaL observed by us in healthy canine ventricular cells was like those reported in rabbit [19,20,21], murine [21,22,23], canine [14,38] and human [14] myocytes under various pathological conditions, such as heart failure, cardiac hypertrophy, ischemia or hypoxia. Here, CAMK2G is linked to heart failure.