As an upstream signaling protein of p53, ataxia telangiectasia mutated (ATM) activates p53 by selective phosphorylation, thereby regulating p53‐dependent signaling pathway12 and cell cycle checkpoints.13 ATM is required for DNA repair and maintenance of genomic homeostasis.14 ATM induces cell senescence in an ATM/p53–dependent signaling pathway in tumor cells15 and endothelial cells.16 ATM can be activated by DNA double‐strand breaks and oxidative stress,17 which are involved in MI18, 19 as well as post‐MI cardiac remodeling.19 The gene discussed is TP53; the disease is neoplasm.