Previous studies have suggested that AML relapse relies on the metabolic reprogramming of the microenvironment, involving cells such as adipocytes19 and BMSCs.8 We have previously shown that, compared with other stromal cells, HSC-niche-forming nestin+ BMSCs20 are preserved and promote AML bioenergetics and chemo-resistance in iMLL-AF9 mice.5 To test whether nestin+ BMSCs are similarly spared in FLT3-ITD;NPMc AML, we measured Nestin-GFP+ cells in Nes-GFP mice21 transplanted with BM cells from FLT3-ITD;NPMc mice (Figures S2A–S2D). Here, NES is linked to acute myeloid leukemia.