Among chronic myeloproliferative disorders, ET is characterized by the greatest heterogeneity in clinical profile, as well as in cellular and molecular levels.19 Autonomous activation of the JAK-STAT pathway in ET patients is progressively increased with the amount of mutant allele.19 Splenomegaly was significantly more frequent when the mutation burden was over 50%, and symptoms due to microvascular disease were present when the mutant allele level was over 25%. This evidence concerns the gene SOAT1 and myeloproliferative neoplasm.