Given the possible association between cell non-autonomous mTORC1 activity and AML pathogenesis (Figure 1), we investigated the role of mTORC1 activity within niche cells in AML progression using niche-specific conditional knockout mice in combination with a well-established MLL-AF9-induced AML murine model that transforms hematopoietic progenitor cells into AML cells. This evidence concerns the gene KMT2A and acute myeloid leukemia.