Schematic diagram describing the effects of the Gas6-Mer axis on endothelial dysfunction in the overlapping pathology between GVHD and TA-TMA Gas6 may be secreted from donor lymphocytes and monocytes in the peripheral blood of patients with GVHD. Gas6 mediated via Mer tyrosine kinase receptor induced platelet aggregation and hypercoagulable status, leading to subsequent TA-TMA onset. In addition, Gas6-Mer signaling pathway enhances progressive endothelial impairment in the common pathology between GVHD and TA-TMA.