Schepers et al. found TPO and CCL3, in conjunction with direct interactions between MSCs and BCR-ABL + leukemic myeloid cells, derive the overproduction of osteoblast derivatives and myelofibrosis during MPN development (Schepers et al., 2013), but bone marrow MSCs from pre-AML MDS and AML patients display apoptosis, deficient proliferation rate, and impairment of osteogenic differentiation (Geyh et al., 2013; Geyh et al., 2016; Li et al., 2020), increased adipogenic potential with improved ability to support survival of leukemia progenitor cells (Azadniv et al., 2020). The gene discussed is ABL1; the disease is leukemia.