The focus on the G6PD-deficient patient group originated from the fact that this genetic disease imparts an immunodeficiency status as suggested in the literature, a decrease in the synthesis of reactive oxygen radicals resulting in diminished activation of the NF-κB pathway [13], increased susceptibility to infection due to neutrophil extracellular trap formation/neutrophil elastase translocation malfunction [14], and increased rate of recurrent infections due to impairment of the microbicidal activity of phagocytes [15]. The gene discussed is NFKB1; the disease is hereditary disease.