The positive regulation of STAT3 transcription by PBX1 binding to its promoter that has been reported in other tissues (Jung et al., 2016) might represent the underlying mechanism through which its expression contributes to MPN development/maintenance; STAT3, part of the JAK/STAT pathway that acts as an effector of the mutations causing MPN, is widely expressed within the hematopoietic system and its transcription is downregulated in the absence of PBX1 in purified HSCs (Ficara et al., 2008). Here, SOAT1 is linked to myeloproliferative neoplasm.