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The fact that two GAPDH inhibitors, HA and iodoacetate, cause NET formation with identical kinetics and morphological changes, at concentrations sufficient to block GAPDH but not at lower concentrations, and that HA-induced NET formation is rescued by 2DG, an inhibitor of glycolysis upstream of GAPDH, or by normalization of the pH, suggest the effects of HA treatment are due to inhibition of GAPDH rather than off-target effects

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