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Additionally, B3GNT3 was found to play a critical role in ferroptosis resistance and PDAC progression, with its knockout suppressing tumor proliferation and migration, which suggests that targeting the N-glycosylation pathway, particularly through the inhibitor tunicamycin, could sensitize PDAC cells to ferroptosis and improve treatment outcomes, though further research is needed to refine such approaches due to the potential cytotoxicity of off-target effects in translational platforms