We previously showed that mammalian Hippo kinase Mst1 phosphorylates Bcl-xL at Serine 14 (Ser14) in cardiomyocytes in response to oxidative stress, which disrupts its interaction with the pro-apoptotic protein Bax, thereby increasing the abundance of active Bax, apoptosis, and myocardial ischemia/reperfusion (I/R) injury in mice3,4. This evidence concerns the gene BAX and myocardial ischemia.