We have previously suggested that the decrease in mitochondrial Bcl‐xL content observed at the end of ischemia could be responsible for cytochrome c release.8 Loss of this antiapoptotic protein could unmask the activity of proapoptotic proteins such as Bax and Bak whose genetic deletion provides powerful protection against reperfusion injury.12 However, here we show that although IP prevented the increased permeabilization of the OMM to cytochrome c (Figure 2), it did not prevent the decrease in Bcl‐xL (Figure 3A and 3B). The gene discussed is BAX; the disease is ischemia.