Given the fundamental role of DCs in shaping immune inflammatory responses in skin it is not surprising that the clinical benefit of several conventional anti-psoriasis therapies, including psoralen and ultraviolet A (PUVA) [135], narrow-band ultraviolet B (NR-UVB) [111,136,137] as well as cyclosporine therapy [22] correlates with a significant decrease in DDC numbers and/or the expression of DC-derived proinflammatory mediators iNOS, TNF, IL12/23p40 and IL-23p19 in psoriatic skin. The gene discussed is TNF; the disease is psoriasis.