G6PD catalyzes the rate-limiting step of the oxidative pentose-phosphate pathway, generating NADPH and pentose phosphates essential for fatty acid and nucleic acid synthesis. The enzyme also converts NAADPH back to NAADP, promoting calcium signaling during T cell activation. G6PD deficiency is the most common human enzyme defect, affecting over 400 million people worldwide, with a distribution paralleling malaria endemicity 1. The disorder is X-linked and caused by mutations in the G6PD gene; approximately 140 mutations have been identified, most involving single base changes 1. Clinical manifestations include neonatal jaundice, acute hemolytic anemia triggered by oxidative stressors (infections, specific medications, foods), and in some variants, congenital non-spherocytic hemolytic anemia 1. The protective effect against malaria results from impaired parasitic nucleotide synthesis; G6PD-deficient red blood cells show markedly reduced pentose phosphate production and glutathione depletion, inhibiting parasite growth 2. Recent evidence suggests G6PD loss triggers dopamine oxidation and neuronal degeneration in Parkinson's disease through reduced NADPH and glutathione availability 3. Management focuses on preventing hemolysis through avoidance of oxidative triggers; evidence-based guidelines identify only seven medications (dapsone, methylene blue, nitrofurantoin, phenazopyridine, primaquine, rasburicase, toluidine blue) requiring strict avoidance 4.