Rab7a may be activated by multiple mechanisms through a GEF such as Ccz1 [35–37], reducing TBC1D15 (GAP protein) levels as shown in vitro [49, 56] and in a mouse model of myocardial infarction [57], or through post-translational protein modifications (reviewed in [58]). This evidence concerns the gene RAB7A and myocardial infarction.