The degree of ACE2 extracellular shedding by ADAM-17 in the form of soluble ACE2 (sACE2, the complete N-terminal ectodomain of the enzyme) revealed a significant association with acute myocardial infarction and circulatory shock in COVID-19 patients, because elevation in sACE2 reflects cellular depletion of ACE2 and diminished tissue protection against Ang II-mediated microvascular damage [43]. This evidence concerns the gene ACE2 and COVID-19.