ATP2A1 and myopathy: Furthermore, it is likely that in combination with the splicing defects in other muscle genes involved in calcium handling (Serca1) and excitability (Clcn1), the mitochondrial damage observed in the CaV1.1ΔE29/ΔE29 mice might be aggravated, and thus contribute to the myopathy (Tang et al., 2012).