Intratumoural Escherichia-Shigella- and Enterobacteriaceae-derived LPS promoted NSCLC progression via the TLR4-mTOR-NF-κB-IL-6 axis, whereas the addition of the mTOR inhibitor rapamycin significantly suppressed LPS-induced tumor proliferation. This evidence concerns the gene TLR4 and non-small cell lung carcinoma.