In addition, fibroblasts from patients with PD with the G2019S LRRK2 mutation showed excessive activation of the MAPK1/3 pathway [38], and knockdown of long noncoding RNA SNHG1 can improve apoptosis, oxidative stress, and inflammation in PD models by inhibiting the miR-125b-5p/MAPK1 axis [39], which indicates that MAPK1 is involved in the pathogenesis of PD. This evidence concerns the gene MAPK1 and Parkinson disease.