An intriguing observation here is that Suv39h1 deficiency seems to confer bigger advantage to mice in terms of survival, infarct size, post-MI heart function and ROS levels than Suv39h2 deficiency (Fig. 3), all of which could probably be attributed to the fact that SUV39H1 acts as a more potent repressor of Sirt1 transcription (Figs 5 and 6). Here, SUV39H2 is linked to myocardial infarction.