In line with other models of LV hypertrophy and diastolic dysfunction (Cho et al., 2017), in human HCM myocardium the ion-channel genes with the most severely depressed expression were Ito and IK1 (Coppini et al., 2013): this might be a consequence of the increased activity of Ca2+/calmodulin-dependent protein-kinase II (CaMKII) in HCM cardiomyocytes (Coppini et al., 2013), which is able to down-regulate Ito and IK1 currents by reducing the expression of functional channels (Wagner et al., 2009). Here, CAMK2G is linked to cardiac hypertrophy.