Since past studies have reported that 15-keto-PGE2 could induce cell death and is a natural PPARγ ligand and that activation of PPARγ inhibited cancer cell proliferation through increasing ROS [4, 44, 45], we suspected that the tumor-suppressor effect of PTGR2 silencing was mediated through increased 15-keto-PGE2 and possibly through PPARγ. This evidence concerns the gene PPARG and neoplasm.