By performing histopathological evaluations and gene expression and computer-assisted immunohistological studies on skin biopsy samples from TNF-α inhibitor-induced skin lesions, Stoffel et al. found increased IFN-α and Th1 cytokine expression, particularly IFN-γ expression, in both eczematous and psoriasiform eruptions caused by TNF-α inhibitors, whereas Th17 predominated in conventional psoriasis, and Th2 predominated in conventional atopic eczema [62]. The gene discussed is IFNA1; the disease is psoriasis.