This model reproduced several clinical hallmarks of eczematous dermatitis including T cell-induced keratinocyte apoptosis and impaired epidermal barriers, upregulation of intercellular adhesion molecule-1 and neurotrophin-4, and increases in the production of proinflammatory cytokines (IL-1α and IL-6) and chemokines (IL-8, IP-10, TARC, MCP-1, RANTES, and eotaxin) (Engelhart et al., 2005). The gene discussed is IL1A; the disease is atopic eczema.