NETosis also appears to be altered in cases with diabetes [for a recent review, refer to Ref. (15)]. Such an instance was first noted when investigating infections with Burkholderia pseudomallei, which appear to be more prevalent in diabetic patients due to a defect in NETosis (27). Joshi et al. noted that while culture (24 h) of isolated neutrophils under high glucose (HG) conditions (30 mM) led to increased NET formation. This was reduced upon subsequent treatment with either LPS, PMA, or TNF-α (28), a feature also recently observed by Carestia and colleagues in an examination of neutrophils isolated from cases with T2DM (29). This is in contrast to the report by Menegazzo and colleagues, who observed that treatment of freshly isolated neutrophils with HG (25 mM) led to enhanced spontaneous NET formation in culture, which was further augmented upon treatment with PMA (30). These authors also noted that the concentrations of NETs or neutrophil-derived products, such as circulating nucleosomes, dsDNA, or neutrophil elastase (NE), were elevated in the plasma of T2DM patients when compared to controls (30). The latter approach was exploited by Wang and colleagues in a study to determine whether NETosis was altered in cases with T1DM (31) and in recent examinations of NETosis in cases with T2DM undergoing therapy (29, 32). While the use of such assays will no doubt remain contentious, and while it is indisputable that such markers are not exclusively of NETotic origin, a number of other studies have suggested they can serve as surrogates to monitor NETs activity under a variety of inflammatory conditions, including RA or PE (24, 33).