Consistent with this hypothesis, TNF-α inhibition has been shown to induce increased expression of IFN-stimulated genes in patients with systemic-onset juvenile idiopathic arthritis [51], and immunohistochemical staining of skin biopsy specimens for myxovirus-resistance protein A (MxA), a surrogate marker of lesional type I IFN activity, showed greater staining in TNF-α inhibitor-induced psoriasis than in psoriasis vulgaris [52]. The gene discussed is TNF; the disease is juvenile idiopathic arthritis.