This paper proposes a comprehensive two-stage anti-cancer hypothesis. In the first stage, we combine Pyrroloquinoline quinone (PQQ), Coenzyme Q10 (CoQ10), Astragalus Polysaccharide (APS), and an Nicotinamide adenine dinucleotide (NAD)+ supplement. Based on the characteristic mitochondrial functional defects of cancer cells, this combination selectively accumulates within them: PQQ and CoQ10 become a metabolic burden due to ineffective utilization, while APS and NAD+ further enhance glycolytic metabolism, collectively pushing cancer cells into a high reductive stress state. Cells in this state become extremely sensitive to subsequent Hyperbaric Oxygen (HBO)therapy, which triggers a catastrophic intracellular Reactive Oxygen Species (ROS) burst and death. Survivors, having activated the Nuclear factor erythroid 2-related factor 2 (NRF2) antioxidant program, upregulate Heme Oxygenase-1 (HO-1), causing a transient surge in intracellular free iron. Timely application of an NRF2 activator then expands the iron pool, exploiting the delayed iron export window to induce Ferroptosis. Crucially, the same combination enhances mitochondrial biogenesis and antioxidant defenses in normal cells, thereby protecting them. In the second stage, the metabolic intervention clears systemic lactate, reverses tumor microenvironment immunosuppression, polarizes macrophages towards the M1 phenotype, and forces residual cancer cells to switch to Oxidative Phosphorylation (OXPHOS), upregulating Major Histocompatibility Complex class I (MHC-I) and CD1d antigen presentation.This renders them susceptible to complete eradication by a multi-layered immune surveillance network comprising CD8⁺ T cells, Natural Killer (NK)cells, CD4⁺ T cells, and invariant Natural Killer T (iNKT) cells capable of circumventing immune checkpoints. This hypothesis provides a theoretical framework for a systemic solid tumor treatment that is theoretically on-target, low-toxicity, and capable of overcoming resistance.