Itsrole in lung cancer is less studied.However, in NSCLC cell lines, activation of PPAR-β/δ with GW501515 increasedproliferation via stimulation of PI3-kinase/Akt signaling resulting inincreased recognition of prostaglandin E2 via transcriptionalupregulation of its EP4 receptor [47].This contrasts PPAR-β/δ with PPAR-γ whose activation is consistently associatedwith inhibition of NSCLC proliferation. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.