Effect of S100A8 deletion in MSCs on disease progression and LSCs in MLL-AF9 leukemic mice. (A) A flow diagram of the MLL-AF9 leukemia model, with S100A8-deficient and control mice as recipients. (B) Leukemic cell infiltration revealed by BM Wright-Giemsa staining in S100A8-deficient and control MLL-AF9 mice. (C) Survival of MLL-AF9 mice in the S100A8-deficient and control groups (n = 8-9). (D) SP size of MLL-AF9 mice in the S100A8-deficient and control groups (n = 4). (E) The proportion of PB leukemia cells in S100A8-deficient and control MLL-AF9 mice (n = 5-6). (F) The proportion of SP and BM leukemia cells in S100A8-deficient and control MLL-AF9 mice (n = 5-7). (G) A flow representation of BM LSCs (YFP⁺c-Kit⁺Gr-1^–) in MLL-AF9 mice. (H) The proportion of PB LSCs in S100A8-deficient and control MLL-AF9 mice (n = 5-6). (I) Proportion of SP and BM LSCs in S100A8-deficient and control MLL-AF9 mice (n = 5-7). (J) Flow representation of BM L-GMPs (IL-7R/Lin^–YFP⁺c-Kit^hiCD34⁺CD16/32^hi) in MLL-AF9 mice. (K) Proportion of L-GMPs of SP and BM of S100A8-deficient vs control MLL-AF9 mice (n = 5-7). (L) Cell cycle of BM LSCs in S100A8-deficient and control MLL-AF9 mice (n = 5-6). (M) Apoptosis of BM LSCs in S100A8-deficient and control MLL-AF9 mice (n = 6). ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. Ctrl,control; KO, knockout; WT, wild-type.