Acquired deleterious SH2B3 variants resulting in increased Janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling are observed in approximately 5% of chronic phase myeloproliferative neoplasms (MPN) either in the presence or absence of canonical MPN driver variants (e.g. JAK2 Val617Phe) [3, 4]. This evidence concerns the gene SOAT1 and myeloproliferative disorder.