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For instance: Sub-toxic doses of nsPEF activate autophagy as a compensatory mechanism to repair membrane damage, but prolonged exposure increases cell death while concomitantly reducing autophagy markers ( Notably, nsPEF can also exert cell cycle-specific effects on tumor cells, such as inhibiting the proliferation of S-phase cells without significantly affecting their viability ( Collectively, these studies reveal the potential of PEFs to exert multi-faceted anti-tumor effects by inducing apoptosis, modulating autophagy, triggering ferroptosis, activating other RCD pathways, and potentially synergizing with chemotherapeutic drugs ( Figure 2 )

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