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Upregulation of GGT activity is primarily dependent on the Ras protein and its downstream effectors, which include extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/AKT and c-Jun N-terminal kinase (JNK) signaling pathways (Fig