André et al noted that major intracellular signaling pathways, including the JAK-STAT pathway, play a role in chronic activation of antigen presenting cells,[26] which can escape suppression by Tregs and generate activated T cells that are refractory to the suppression by Tregs.[27] Following these findings, one may hypothesize that constitutive activation of JAK2 and its downstream pathway in ET may have contributed to the development of ITP in the case presented in this report. Here, SOAT1 is linked to autoimmune thrombocytopenic purpura.