Furthermore, we demonstrated the upstream regulatory mechanism of NEAT1 disorder in lung adenocarcinoma, that is, Galectin-3 activates TLR4/NF-κB signaling, followed by p65 nucleus translocation, ultimately activating NEAT1 expression and promoting lung adenocarcinoma cell proliferation and migration (Fig. 8). The gene discussed is TLR4; the disease is lung adenocarcinoma.