Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most prevalent enzyme disorder, estimated to affect 400 million people worldwide. Mutations in the G6PD gene, situated in the long arm of the X chromosome, result in different G6PD deficiency variants, producing a wide range of biochemical and clinical phenotypes, which can be further distinguished by differences at the molecular levels. Drug related haemolytic anaemia was first observed with the use of Primaquine, and was subsequently discovered to be caused by G6PD deficiency.  The link between G6PD deficiency and malaria is further bolstered by the observation of the global distribution of G6PD deficiency being parallel with that of malaria. This observation led to the suggestion that G6PD deficiency has protective advantage as a defence against malaria. Different G6PD deficiency variants have different propensities to cause haemolytic anaemia on exposure to oxidant drugs. Knowledge of the different biochemical and molecular variants of G6PD deficiency is important not only between people in different continents but even between people in different regions of the same country. G6PD deficiency produces a wide spectrum of clinical disorders, whose observable differences can be due to different oxidant drugs, different infections, and even different age groups.