Previous studies have demonstrated that CDC25B expression is associated with resistance to the antiproliferative effect of PI3K/Akt/mTOR inhibitors [40] and that CDC25B activity is required for the activation of Akt, whereas the inhibition/knockdown of CDC25A reduces Akt-dependent AML cell proliferation [44]. The gene discussed is AKT1; the disease is acute myeloid leukemia.