In non–small cell lung carcinoma (NSCLC) cells, the expression of PPARβ/δ is activated by nicotine through PI3K/mTOR [327], whereas GW501516, a PPARβ/δ agonist stimulates cell proliferation by inhibiting the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), which signals downstream to mTOR [328], picturing an interplay between the two pathways. This evidence concerns the gene MTOR and non-small cell lung carcinoma.