The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein 
kinase (MAPK) family and are activated by environmental stress. JNK is also 
activated by proinflammatory cytokines, such as TNF and IL-1, and Toll-like 
receptor ligands. This pathway, therefore, can act as a critical convergence 
point in immune system signaling for both adaptive and innate responses. Like 
other MAPKs, the JNKs are activated via the sequential activation of protein 
kinases that includes two dual-specificity MAP kinase kinases (MKK4 and MKK7) 
and multiple MAP kinase kinase kinases. MAPKs, including JNKs, can be 
deactivated by a specialized group of phosphatases, called MAP kinase 
phosphatases. JNK phosphorylates and regulates the activity of transcription 
factors other than c-Jun, including ATF2, Elk-1, p53 and c-Myc and 
non-transcription factors, such as members of the Bcl-2 family. The pathway 
plays a critical role in cell proliferation, apoptosis, angiogenesis and 
migration. In this review, an overview of the functions that are related to 
rheumatic diseases is presented. In addition, some diseases in which JNK 
participates will be highlighted.