Here, the JNK pathway is activated via phosphorylated c-Jun in the striatum and in the substantia nigra; this appears not to be correlated with the loss of neuronal cell bodies but might represent a response to damage/loss of axonal terminals (Willesen et al. 2002), as has been corroborated by the finding that c-Jun is activated in dopaminergic neurons from PD patients. This evidence concerns the gene JUN and Parkinson disease.