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Acetoacetyl-CoA is then converted to 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA), followed by acetoacetate, and finally, -hydroxybutyrate (BHB) is supplied as a substrate for neuronal ATP synthesis

Furthermore, exploiting antioxidant vulnerabilities through aldehyde dehydrogenase (ALDH) inhibition with agents like disulfiram, or glutathione peroxidase 4 (GPX4) inhibition, can induce ferroptosis specifically in DTP populations, further reducing residual tumor burden (Raha et al., 2014)

CONCLUSION In summary, we find that glutathione metabolism plays an essential role in pancreatic cancer aggressiveness, supporting CSC survival, self-renewal and chemoresistance