Other studies have reported that peri-arteriolar Nes+ BMSCs reside both in AML patients and in MLL-AF9 mice [124,125] and this subpopulation exhibited abnormal proliferation and differentiation coinciding with depletion of the quiescent Nesperi population, and establishes an abnormal niche which trigger HSC exhaustion [124] maybe through reducing expression of VLA-4, VCAM-1, CXCL12, Ang-1, SCF, and TGFβ-1 [126] and increased expression of OPN. The gene discussed is NES; the disease is acute myeloid leukemia.