These findings add further knowledge to recent studies showing that increasing levels of ADAM17 substrates (ACE2, TNFR1 and TNFR2) are associated with adverse clinical outcomes in COVID-19 patients [8] and that inhibition of ADAM17 activity in vitro dose-dependently reduces SARS-CoV-2 infection [7]. This evidence concerns the gene TNFRSF1B and COVID-19.