In MI, loss of the ACE2 gene leads to ventricular remodelling, increased myocardial fibrosis, neutrophilic infiltration and superoxide production via up‐regulation of matrix metalloproteinase (MMP) 2, MMP9, interferon‐γ, IL‐6 and chemokines as well as regulation of phosphorylation of the extracellular regulated protein kinase (ERK) 1/2 and c‐Jun N‐terminal kinase (JNK) 1/2 signalling pathways.44 The gene discussed is ACE2; the disease is myocardial infarction.