Furthermore, either TBC1D15 mutant lacking Fis1 binding or RAB7 GAPase activation failed to modulate lysosomal acidification, mitophagy flux activation and cardioprotective effects mediated by TBC1D15, indicating an essential role of mitochondria-lysosome contacts in acute MI-induced lysosomal dysregulation, mitophagy flux blockage and cardiac abnormalities. This evidence concerns the gene TBC1D15 and myocardial infarction.