The interaction between VLA-4–expressing AML cells with fibronectin on MSCs has been correlated with adverse outcomes and recurrence in AML, as this interplay causes increased drug resistance mediated by intracellular activation of the phosphatidylinositol-3-kinase (PI-3K)/AKT/Bcl-2 pathway [127]. The gene discussed is AKT1; the disease is acute myeloid leukemia.