PROS1 and endothelial dysfunction: In summary, there are three main hypotheses about the possible immunological pathogenetic pathways that initiate and drive MIS-C development: genetic predisposition concerning the ability of T cells to bind to S-protein; direct viral effect leading to endothelial dysfunction, platelet activation and multiorgan damage and the leading theory of maladaptive postinfectious response at different levels—APCs-T cells interactions, antigen-antibody-mediated cytokine storm, superantigen Vβ31-3T cells activation, formation of immune complexes or autoantibodies, etc.