More precisely, Naka et al. describe that FOXO3a plays an essential role in the maintenance of CML-LSCs in a CML-like myeloproliferative disease mouse model [47] and that TGF-β activates AKT in LSCs by controlling FOXO3a localization [47]. The gene discussed is TGFB1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.