have demonstrated that nanoparticle delivery of FOXM1 stimulates lung angiogenesis and alveolarization during recovery from neonatal hyperoxic injury.[45] Shuo et al. have found that Foxm1 overexpression not only attenuates acute myocardial infarction injury, but it also prevents ventricle remodeling and infarct expansion.[46] Here, we have generated a TAM‐inducible, CM‐specific, Foxm1‐transgenic mouse line to demonstrate that CM‐specific Foxm1 overexpression attenuates I/R injury‐induced cardiac damage and remodeling by preserving mitochondrial bioenergetics. This evidence concerns the gene FOXM1 and myocardial infarction.