Evidence from non-clinical trials indicates that eicosanoids and lipid mediators may are involved in cancer development surrounding inflammatory and stromal cell responses [43] and provides a reference for the potential benefits of NSAIDs in cancer chemotherapy via activation apoptosis [44] and modulation tumor autophagy through the PI3K/Akt/mTOR, MAPK/ERK1/2, P53/DRAM, AMPK/mTOR, Bip/GRP78, CHOP/GADD153, and HGF/MET signaling pathways and inhibition lysosome function, leading to p53-dependent G1 cell-cycle arrest [45]. The gene discussed is MET; the disease is cancer.