In accord with this, ASK1 was activated only by ischemia (associated with moderate levels of ROS) in perfused hearts, but not on reperfusion (with much higher levels of ROS).29 Our data for ASK1 are consistent with previous studies of myocardial infarction in ASK1 knockout mice.20 Here, ASK1 deletion reduced the percentage of apoptotic cardiomyocytes particularly in the peri-infarct zone, a region likely to be subjected to lower ROS levels than cells in the infarct zone itself. Here, MAP3K5 is linked to myocardial infarction.