In the normal like/disease free BM analyzed, we observed that MCT1 positive cells also localized near the bone trabeculae and MCT4 positive cells are diffuse in BM, reinforcing that metabolic adaptation allows AML M0-M5 to benefit from a natural BM organization driven also by VEGF, as it is already described [27, 46–49]. The gene discussed is SLC16A1; the disease is acute myeloid leukemia.