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By interacting directly with MAPKs, including c-Jun N-terminal kinase 1 (JNK1) and apoptosis signal-regulating kinase 1 (ASK1), GSTs bind the ligand in a complex structure, preventing interactions with their downstream targets [74]

Strategies that deplete GSH, such as using inhibitors like BSO which is inhibitor of -glutamylcysteine synthetase (-GCS) , the rate-limiting enzyme in glutathione (GSH) synthesis or by combining prodrug activation with GSH depletion in nanosystems, have shown promise in overcoming MDR and improving chemotherapy effectiveness [72]

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