The SAPK/JNK pathway is homologous to the MAPK pathway in its overall form but is activated by largely distinct stimuli (1). A variety of extracellular stimuli activate the JNK/SAPK pathway including inflammatory cytokines, UV light, inhibitors of protein synthesis and osmotic stress (1–5). Inflammatory cytokines such as TNFa and IL1 appear to activate this pathway via the Rac/Rho family of small GTP binding proteins, whereas inhibitors of protein synthesis and UV light appear to act independently of Rho and Rac (6). Activated MEKK1 phosphorylates SEK1 (also known as MKK4), which in turn activates SAPK (also known as JNK). SAPK binds tightly to the N-terminal region of c-Jun and ATF-2. It phosphorylates c-Jun at Ser63 and Ser73, and ATF-2 at Thr69 and Thr71 (5).