The mutations all share the characteristic of affecting the JAK‐STAT signal transduction pathway generating the classic MPN phenotype, with activation and proliferation of the haematopoietic progenitor cell, and uncontrolled production of different terminal blood cell quantities, depending on MPN subtype and mutation type (Shallis et al., 2020). This evidence concerns the gene SOAT1 and myeloproliferative neoplasm.