Hypermethylation of the JAK-STAT inhibitor suppressor of cytokine signaling (SOCS) 1 has been shown by independent groups and downregulation of SOCS-3 as well as src homology region 2 domain-containing phosphatase 1 (SHP1) has been found to be associated with promoter methylation in MPN patients[12,16] Further evidence of involvement of epigenetic dysregulation in MPN pathogenesis evolve from the findings of loss-of-function mutations in enhancer of zeste homolog 2 (EZH2), ASXL1 and TET2 with resulting deregulation in both DNA methylation and chromatin structure[17]. Here, SOAT1 is linked to myeloproliferative disorder.