AML cells induce osteogenic differentiation but inhibit adipogenic differentiation of MSC leukemia growth, whereas normal hematopoiesis is favored by AML-secreted exosomes and pro-inflammatory IL-1, which promote the expansion of AML progenitors and disease progression by activating the IL-1/p38MAPK pathway. The gene discussed is IL1B; the disease is acute myeloid leukemia.