Classical Philadelphia chromosome-negative (Ph-neg) myeloproliferative neoplasms (MPN) are clonal hematopoietic disorders with a unique pathogenic mechanism in which mutually exclusive driver mutations in calreticulin (CALR), MPL, and JAK2 trigger the activation of Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signaling axis [1]. Here, SOAT1 is linked to myeloproliferative neoplasm.