TNF and gastritis: Phosphatidylinositol 3′-kinase-Akt (PI3K-Akt), tumor necrosis factor (TNF), mammalian target of rapamycin (mTOR), Toll-like receptor, chemokine, mitogen-activated protein kinase (MAPK), nuclear factor-kappa B (NF-kB), Hypoxia-inducible factor 1 (HIF-1), and transforming growth factor-beta (TGF-beta) signaling pathways were selected as the main pathways associated with gastritis treatment (Figure 7).