We previously demonstrated that CNF1 also activates FAK, and that FAK activation reverses the SMG-induced inhibition of tumor cell proliferation and metastasis by modulating the mTORC1 and AMPK pathways [32]; overcomes SMG-promoted cell apoptosis via the mTORC1/NF-κB and ERK1/2 pathways [33]; and results in SMG-inhibited OBD via the transcriptional Wnt/β-catenin-BMP2-COL1 pathway [31]. The gene discussed is NFKB1; the disease is neoplasm.