The pathophysiology of thrombocytopenia in this setting is multifactorial, involving platelet sequestration in the spleen due to portal hypertension, impaired platelet production from bone marrow suppression, and inappropriately reduced TPO production [3]. Furthermore, in a study done by Satoh et al., B cells produced significantly more GPIIb/IIIa in ESLD patients compared to controls, potentially increasing the risk of ITP and contributing to severe thrombocytopenia [5]. This evidence concerns the gene TPO and autoimmune thrombocytopenic purpura.