Furthermore, we do not yet know if the anti-inflammatory effect of chronic immunosuppressive therapy plays an undetermined role in the ‘cell damage cascade’ triggered by an uncontrolled cytokine storm and lymphocyte–macrophage activation, as has already been speculated in the literature [20, 21]. Indeed, some evidence suggests that lung damage in the severe forms of the disease is essentially due to immune hyperactivation rather than viral pathogenesis per se [6].