AKT1 and cancer: As no activation of the CAGA reporter assay was achieved by TGF-β treatment, we also speculate that IGFBP2 via activation of Akt and/or Yap mediated stabilization of Smad7, as recently described for cancer stem cells (Machida et al. unpublished), might interfere with cytostatic TGF-β/Smad signaling.