By exploiting an MPN mouse model bearing the JAK2V617F mutation, we demonstrated that PBX1 expression in JAK2V617F HSCs is necessary to sustain MPN (Muggeo et al., 2021), in accordance with a previous report indicating that its overexpression in JAK2V617F HSCs contributes to sustaining an MPN phenotype in animal models (Shepherd et al., 2018). Here, PBX1 is linked to myeloproliferative disorder.