Increased activity of ADAM17 could, apart from inducing increased ACE2 shedding, play a pivotal role in inducing COVID-19-associated lung inflammation by shedding membrane-bound tumor necrosis factor (TNF) alpha, interleukin (IL) 6R, TNF receptors (TNFRs) and other pro-inflammatory mediators, thereby contributing to the cytokine storm observed in severe COVID-19 [6]. This evidence concerns the gene ACE2 and COVID-19.