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The nonenzymatic functions of GSTs involve their interactions with cellular proteins, such as, Jun N-terminal kinase,(JNK), tumor necrosis factor receptor-associated factor-2 (TRAF2), apoptosis-signal-regulating kinase 1 (ASK), serine/threonine kinases (PKA, PKC), and tissue transglutaminase 2 (TGM2), during which, either the interacting protein partner undergoes functional alteration or the GST protein itself is post-translationally modified and/or functionally altered [53], [74]

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Highly lipophilic compounds have an increased risk of being poorly soluble, quickly metabolized and promiscuous binders, whereas more polar compounds often are less permeable

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