Mechanisms underpinning the effects of BCL3 on breast cancer cell migration include NF-kB/BCL3 mediated transcriptional regulation of N-cadherin and cdc42 [112] and protein stabilization of SMAD3 induced by TGF-β [14] while in a mesenchymal subset of glioblastoma this TGF-β / SMAD3 axis drives BCL3 transcription – suggesting that in some cancer contexts a positive feedback exists between BCL3 and SMAD3 to drive disease progression, mediated ultimately through upregulation of BCL3. The gene discussed is SMAD3; the disease is glioblastoma.