While several postulated mechanisms exist, including direct infiltration of cells and platelets with defective marrow microenvironment, decreased thrombopoietin production from viral-mediated liver damage, platelet aggregation and consumption with the formation of microthrombi following pulmonary endothelial damage and immune system-mediated platelet destruction, what has been consistent across the literature is the response of COVID-19 induced thrombocytopenia to short courses of corticosteroids and intravenous immunoglobulin [16]. Here, THPO is linked to COVID-19.