Since a procoagulant state and hyper-fibrinolysis co-exist in COVID-19 (Tang et al., 2020b), we assume that the increased fibrinolysis boosts the infectivity of SARS-CoV-2 via the plasmin-mediated pathway. In addition, plasmin elicits a pro-inflammatory response by activating macrophages (releasing IL-6, and TNF) and increases PAR2-TLR4 signaling (Li et al., 2007; Antoniak and Mackman, 2014). This evidence concerns the gene IL6 and COVID-19.