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mice were 3.7 AE 0.3, and 3.7 AE 0.4, respectively. In both TNFa suppressed mice, a hyperinflammatory syndrome associated with necrotic lesions was observed. Conclusions: Neither genetic deletion of TNFa nor treatment with a TNFa scavenger prevented skin hyperinflammation in CGD mice. Thus, unlike as previously suggested, TNFa probably does not represent a potential target for the treatment of CGD hyperinflammation. However, our results were obtained in skin hyperinflammation and future research will have to investigate the similarities and differences between hyperinflammation in the skin and the colon.