A fascinating development of this investigative focus on late Na+ current and CaMKII is the observation that CaMKIIδc interacts with the neuronal form of the Na+ channel (Nav1.8) normally expressed in human ventricular cardiomyocytes at low levels but upregulated several fold in HF (Dybkova et al., 2018). The gene discussed is SCN10A; the disease is hydrops fetalis.