Nevertheless, with apoptosis genes upregulated and cell cycling genes downregulated in BMMNCs and HSPCs in VEXAS, and functionally, both BMMNCs and CD34+ HSPCs from patients formed fewer colonies than did cells from healthy individuals (Figure S7B), myeloid progenitors and HSPCs in VEXAS likely exhibited defective proliferation and differentiation, reflecting the ineffective hematopoiesis typical of MDS. Here, CD34 is linked to myelodysplastic syndrome.