Although the pathophysiological mechanisms underlying such persistent or delayed clinical manifestations of the convalescent phase are still a matter of study, several mechanisms have been proposed to have a role in the pathogenesis of PASC and long-term thrombotic complications, including the virus-induced downregulation of ACE2, inflammatory cytokines produced by activated leukocytes, endothelial dysfunction, hypercoagulability, and inflammation [45]. This evidence concerns the gene ACE2 and thrombophilia.