This phenomenon may occur because the primary pathogenic agent of COVID-19, SARS-CoV-2, enters circulating neutrophils via binding to angiotensin-converting enzyme 2 (ACE2) and priming of the spike (S) protein by transmembrane protease serine 2 (TMPRSS2), where it replicates, activates NETosis, and releases NETs that further induce microthrombosis and vasculopathy (71, 123, 124). Here, TMPRSS2 is linked to COVID-19.