CDC25 inhibitors can inhibit AML cell proliferation induced by integrin adhesion to fibronectin [87]; this integrin-initiated growth enhancement seems to be at least partly mediated through activation of PI3K-Akt-mTOR signaling, and its inhibition is thus an additional observation suggesting a functional interaction between CDC25 and PI3K/Akt/mTOR. The gene discussed is FN1; the disease is acute myeloid leukemia.