As previously reported, the mechanism of VITT has been clearly explained because the immune thrombocytopenia and related thrombocytolysis promote thrombus formation in a similar way for HITT; antibodies against PF4-heparin complexes were identified during both diseases, thus confirming that pathophysiological mechanisms of HITT and VITT are similar. Here, PF4 is linked to autoimmune thrombocytopenic purpura.