In fact, in patients with hereditary deficiency of NOX2 and in patients with upregulation of NOX2 such as those with diabetes, platelet production of 8‐iso‐PGF2α was reduced and increased, respectively.3,8 Such interplay was reinforced by an in vitro study in which platelet incubation with a specific inhibitor of NOX2 was associated with impaired production of 8‐iso‐PGF2α.3 We speculated that these 2 settings were unique in investigating if urinary 8‐iso‐PGF2α could reflect platelet production of 8‐iso‐PGF2α. Here, CYBB is linked to hyperinsulinemic hypoglycemia, familial, 4.