To understand if alterations of BMSC osteogenic commitment can be specifically caused by AML infiltration in healthy BM, we evaluated the expression of tissue non-specific alkaline phosphatase (TNAP), an early osteogenic marker upregulated on AML-derived BMSCs (24), on normal BMSCs co-cultured with different AML cell lines (HL-60, KG-1, THP-1, U-937) in an in vitro 2D system, as described in Figure 1A. The gene discussed is ALPL; the disease is acute myeloid leukemia.