Animal models in which OGG1 has been shown to promote inflammation include contact hypersensitivity (skin inflammation; [18]), endotoxin shock (generalized, “whole body” inflammation) [18], asthma [46], Pseudomonas infection [47], hypoxia-reoxygenation-induced neuroinflammation [48] and TNF-induced lung inflammation [23]. The gene discussed is TNF; the disease is dermatitis.