Reduced expression of c-Myc does not rescue the self-renewal defect of HSCs in mice. (A) Flow cytometric analysis of donor (CD45.2⁺CD45.1⁻)– and WT competitor (CD45.2⁺CD45.1⁺)–derived PB cells in recipient mice (CD45.2⁻CD45.1⁺) 1 to 5 months after transplantation. (B) Representative diagrams of PB flow cytometry data for the fifth month. (C) Flow cytometric analysis of donor– and WT competitor–derived PB cells in different lineage populations from the recipient mice. (D) Representative diagram of flow cytometric analysis of myeloid cells in mice 5 months after transplantation (n = 5 for each group). (E) A model of c-Myc–mediated intrinsic and extrinsic regulation of HSC fate. c-Myc mediates the function of the Wnt/β-catenin signaling pathway in endothelial cells through IL6 secretion. c-Myc controls HSC quiescence and quiescence by directly activating expression of Nr4a1, Nr4a2, and Jmjd3.