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Chronically transfused patients may be adversely affected by nonoptimal RBC transfusions, and patients with sickle cell disease, in particular, are exposed to a significant number of transfusions from G6PD-deficient donors (i.e., up to 12%) (25)

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Under conditions of hypoxia, nutrient deprivation, or impaired mitochondrial function, cancer cells modulate NADPH and GSH levels through key metabolic pathways such as the pentose phosphate pathway (PPP), FAO, and glutamine metabolism, thereby establishing a metabolic–redox feedback loop [39,40,41]