In fact, under these conditions, therapeutic cytoreduction of AML blasts can cause a drop in the BM levels of TNFα and in turn lead to a post-treatment enrichment of BM CD31+Sca-1high ECs and arterioles with a consequent increase in the endothelial miR-126 supply to LSCs, which, once enriched in miR-126, are more resistant to therapy[31, 49]. The gene discussed is TNF; the disease is acute myeloid leukemia.