The Ca2+-activated protease calpain has been variously suggested to be responsible for the cTnI C-terminal cleavage observed during ischemia/reperfusion (I/R) (9), which may contribute to stunning (9, 10), or for the N-terminal cleavage that has been seen in chronic simulated microgravity (11), heart failure (12), and even in healthy hearts (11). This evidence concerns the gene TNNI3 and heart failure.