Zhao et al. (2019) found that miR-4532 was significantly overexpressed in AML cell lines compared with CD34+ hematopoietic stem cells (HSCs) and enriched in AML cell exosomes. Exosomal miR-4532 could be transferred into HSCs and repress normal HSC hematopoiesis via activation of the LDOC1-dependent STAT3 signaling pathway. Hornick et al. (2016) found that exosomes derived from AML cells could destroy hematopoietic function through transferring miR-150 and miR-155 to hematopoietic stem cells and promote AML development. The gene discussed is CD34; the disease is acute myeloid leukemia.