in various neurodegenerative [3], neuromuscular [4], and cardiac disorders [5,6]. The development and testing of Calpain inhibitors as therapeutic agents is the subject of intense ongoing research [3,5,7]. One emerging target of Calpain cleavage under pathophysiological conditions is Junctophilin-2 (JP2) [8,9]. Recently, we systematically analyzed the JP2 cleavage products as a function of Calpain-1 versus Calpain-2 proteolytic activities [10]. Together with newly