Previous data obtained on PARK2-PD fibroblasts harboring a compound heterozygous deletion (del exon2-3/del exon3) in PARK2 displayed mitochondrial defects and Peroxisome proliferator-activated receptor Gamma Coactivator 1-alpha (PGC-1α) dysfunction [39], severe ultrastructural abnormalities, mainly in mitochondria and cytoskeleton [39,55], and altered expression level of several proteins involved in cytoskeleton structure dynamics, Ca2+ homeostasis, oxidative stress response protein and RNA processing [56,57]. Here, PRKN is linked to Parkinson disease.