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Activation of oncogenes and loss of tumor suppressors lead to the increased production of superoxide via mitochondria and NADPH oxidase (NOX) pathways ( 2 O 2 ), a more stable and stronger oxidizing molecule, through the action of superoxide dismutase enzymes (SOD)

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It was supposed that GST29 likely prevents plant cell disruption and death caused by highly toxic radicals that accumulate during infection, localizing thereby the host response during HR (Mauch and Dudler, 1993)

Combining it with tirzepatide adds a receptor target (amylin) without the glucagon component that retatrutide provides

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