NET formation can be inhibited by NAC and DPI, indicating the involvement of oxidative stress and NOX. A metabolic shift towards the PPP is required for the NET formation induced by amyloid fibrils and PMA [93]. G6PD-derived NADPH can serve as a substrate for NOX, which generates superoxide and stimulates NET formation [17]. Neutrophils from individuals with the G6PD Taiwan-Hakka variant are equally effective as normal individuals regarding NET formation [94]. However, defective NET formation and NOX activity are observed in neutrophils of individuals with severe G6PD deficiency [95]. The absence of NET formation is found in NOX deficiency associated with chronic granulomatous disease (CGD). Severe G6PD deficiency may mimic impaired NOX resulting in dysfunctional NETs.