After the confirmation of a Ca2+ overload state in our model and based on previous evidence of CaMKII autophosphorylation in a rat model of TS1 (ref. 8), we investigated, in our model, the presence of alterations of NaV1.5, a well-known downstream target of CaMKII (ref. 46). The gene discussed is CAMK2G; the disease is Timothy syndrome type 1.