Translocation and/or activation of Bcl2 family members is known to play a key role in OMM permeabilization, and it has recently been shown that the deletion of Bax and Bak dramatically reduces necrotic injury during myocardial infarction in vivo.12 We previously showed that neither Bax nor Bak levels increased in mitochondria after ischemia, but there was a decrease in the antiapoptotic protein Bcl‐xL that might account for OMM permeabilization.8 The data of Figure 3A and 3B confirm this loss but reveal that it was not prevented by IP. The gene discussed is BCL2; the disease is ischemia.