Phosphorylated CaMKII and CaMKII mediated increased phosphorylation of serine 571 was observed in ventricular myocytes of non‐ischaemic HF patients and in canine post infarct border zone, but not in transgenic mice AC3‐I expressing CaMKII inhibitor.122 CaMKII‐mediated NaV1.5 channel phosphorylation and regulation exhibits both gain‐of‐function (increased late INa) and loss‐of‐function (decreased availability) effects, indicating complex regulation by phosphorylation. This evidence concerns the gene CAMK2G and hydrops fetalis.