Since the discovery of the role of the three driver mutations (JAK2, CALR and MPL) and the constitutive activation of the JAK/STAT pathway in myeloproliferative neoplasms, the disease has been wrongly considered to be molecularly elucidated, and efforts have mainly focused on the implementation of JAK inhibitors in the clinical setting. Here, SOAT1 is linked to myeloproliferative disorder.