It is tempting to speculate that the survival pathways upregulated at BP in the two MDS groups are induced both by the specific mutations present in the two MDS subgroups at baseline (for example, RUNX1 mutations are known to activate the NF-κB pathway24) and by changes in the microenvironment occurring at BP (for example, TNF upregulation in the microenvironment of GMP-pattern MDS further enhances NF-κB pathway activation25). Here, TNF is linked to myelodysplastic syndrome.