The oncogenic transformation can be promoted by persistently activated STAT proteins because of several somatic mutations in the JAK-STAT pathway, which have been identified in patients with a variety of diseases, including myeloproliferative disease, polycythemia vera, megakaryoblastic myeloid leukemia, lymphoblastic leukemia, and uterine leimyosarcomas16, and also could cause CRC17. Here, SOAT1 is linked to myeloproliferative disorder.