In cardiac fibrosis, ADAM17 releases ACEII into the extracellular fluid through cleavage, where soluble ACEII converts Ang II to Ang1‐7, unlike the pro‐inflammatory and proliferative properties of Ang II [42, 43] mitigating myocardial fibrosis, myocardial hypertrophy and cardiomyocyte apoptosis by binding to MRSR [44]. This evidence concerns the gene ADAM17 and cardiac hypertrophy.