We demonstrated Galectin-3-induced TLR4/NF-κB signaling activation could contribute to lung adenocarcinoma cell proliferation and migration through p65 nucleus translocation and NEAT1 expression upregulation; Galectin-3/TLR4/NF-κB/NEAT1 path might be another contributor to the hyperproliferation and migration of lung adenocarcinoma cells. The gene discussed is NFKB1; the disease is lung adenocarcinoma.