Our study provides a further mechanistic insight into ASXL1 functions in the BM niche, and how ASXL1 alteration-associated defective niche works in concert with an intrinsic effect of ASXL1 alteration-mediated HSC/HPC defects to promote the pathogenesis of myeloid malignancies. This evidence concerns the gene ASXL1 and myeloid neoplasm.