When c-Abl is activated by oxidative stress in an acute PD model, p38α was identified as the main substrate of c-Abl, and c-Abl-mediated phosphorylation was found to be crucial for the dimerization of p38 (AIMP2) [16], which in turn initiates the expression of IL-1, IL-6, TNFα. This evidence concerns the gene ABL1 and Parkinson disease.