Abstract
The human red blood cell (RBC), with its array of unique features, was once elegantly described as “a marvellous example of functional bioadaptation and an invitation to disaster”.1 The numerous defects in haemoglobins, membrane proteins, and enzymes, which can result in anaemia and severe disease, seem to confirm this prediction. Pyruvate kinase deficiency is a rare disease associated with non-spherocytic congenital anaemia. In glycolysis, pyruvate kinase (PK) catalyses the conversion of phosphoenolpyruvate to pyruvate, with the production of ATP.
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