Therefore, the combined effects of (i) α-DG hypoglycosylation and loss of laminin binding; (ii) β-DG fragmentation carried out, in part, by MMPs with consequent changes in the scaffolding of MAPK signaling; and (iii) nuclear translocation of β-DG resulting in upregulated ETV1 transcription and, in turn, of MAPK-dependent signaling leading to an increase in cell migration, could represent a positive feed-back mechanism driving prostate cancer progression [99]. The gene discussed is ETV1; the disease is prostate cancer.