Cleavage of the S protein by cellular proteases, including furin and TMPRSS-2 (transmembrane protease serine 2), is speculated to play an important role in the infectivity and host range of SARS-CoV-2, although its functional significance regarding how this feature may mediate SAR-CoV-2 transmissibility and pathogenicity is yet be fully elucidated.1 In the context of COVID-19-associated thrombosis, understanding how these structural differences of SARS-CoV-2 may relate to the prothrombotic phenotype of COVID-19 is likely to be of fundamental importance given the significantly higher rates of thrombosis observed in SARS-CoV-2, compared with SARS-CoV and MERS-CoV infections.