Due to these variations between primary AML cells their communication with leukaemia-supporting neighbouring cells in the BM microenvironment will also differ, and the direct effects of PI3K-Akt-mTOR inhibition on the AML cell communications with neighbouring cells will thereby be difficult to predict and may even increase the patient heterogeneity with regard to the final effect of the treatment on the AML cells. The gene discussed is AKT1; the disease is acute myeloid leukemia.