Genetic mutation causes reduced efficiency of the dimerization of G6PD monomers affecting its biological activity; in many cases, the pathological effects of G6PD deficiency were not associated with the reduced expression, but reduced binding energy affecting formation of G6PD homodimers (active form), such as class I G6PD variants, associated with chronic nonspherocytic hemolytic anemia (CNSHA), the most severe phenotypic expression of G6PD deficiency [25]. This evidence concerns the gene G6PD and G6PD deficiency.