In CD133+ lung adenocarcinoma stem cells, we found that gal-1 knockdown significantly reduced COX-2 expression and PGE2 secretion, and the phosphorylation levels of AKT and mTOR, more importantly, exogenous galectin-1 could partially rescue the influence of galectin-1 knockdown. The gene discussed is MTOR; the disease is lung adenocarcinoma.