A previous study showed that cardiac fibroblasts underwent senescence after MI, and p53 deficiency decreased fibroblast senescence as well as cardiac fibrosis in response to MI.8 In the present study, we further showed that ATM was responsible for MI‐induced fibroblast senescence, as ATM haplodeficiency resulted in increased myofibroblast accumulation and fibrosis by suppressing fibroblast senescence, as shown by reduced SA‐β gal staining and p21 and p19 levels (Figure 5). Here, ATM is linked to myocardial infarction.