In line with this idea, muscle-specific overexpression of SERCA1 restores both peak Ca2+ transient amplitude and decay kinetics, as well as dramatically attenuates the dystrophic phenotype in two different muscular dystrophy mouse models (mdx and Sgcd−/− mice; Goonasekera et al., 2011). The gene discussed is ATP2A1; the disease is muscular dystrophy.