For Duchenne Muscular Dystrophy (DMD), the two main hypotheses related to calcium handling abnormalities are membrane fragility/damage (Carson et al., 2016), as reported in the human DMD-hiPSC-cardiomyocyte (Guan et al., 2014; Macadangdang et al., 2015) and mdx mouse (Fanchaouy et al., 2009) model, or altered ion channel function with dysregulation of calcium homeostasis as a direct consequence of the altered dystrophin glycogen complex (DGC) (Zhan et al., 2014). This evidence concerns the gene DMD and Duchenne muscular dystrophy.