To this end, prevention of post-treatment CD31+Sca-1high EC expansion, arteriolar re-vascularization and LSC protection is achievable with pharmacological deprivation of BM endothelial miR-126 (i.e., miRisten), which may represent a novel strategy to overcome non-genetically driven, extrinsic mechanisms of LSC resistance in AML. The gene discussed is PECAM1; the disease is acute myeloid leukemia.