2014), and channel inactivation was reduced (Koenig et al. 2014; Sadeghi et al. 2002; Viola et al. 2014, 2013; Woolf et al. 2006) in dystrophic ventricular cardiomyocytes derived from mdx mice. The mdx mouse (Sicinski et al. 1989) is dystrophin‐deficient and the most commonly used mouse model of DMD. Both the named Ca channel abnormalities (increased current amplitudes and reduced inactivation) will increase the Ca influx into the dystrophic myocyte during an action potential (AP) and thereby enhance the risk of Ca‐dependent arrhythmias and cellular Ca overload (Zhou et al. 1998). Here, DMD is linked to Duchenne muscular dystrophy.