Impaired bacterial phagocytosis and killing in hyperglycemia have been associated with reduced production of lysosomal enzymes, bactericidal/permeability-increasing protein (BPI), and reactive oxygen species, reduced production and activation of elastase, reduced neutrophil extracellular trap (NET) formation and degranulation, as well as glycation-dependent hindrance of C3 binding to bacteria during opsonophagocytosis [18,62–65]. This evidence concerns the gene BPI and Hyperglycemia.