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Our recent study has revealed that calpastatin,an endogenous calpain inhibitor,could not only reprime activity of Cav1.2 Ca2+ channel from run-down in cell-free patches but also directly bind to intracellular C-terminal region of Cav1.2 channel.However,the pathophysiological role of Cav1.2-channel-regulating function of calpastatin was largely unknown.