Taken together, several conclusions can be drawn: 1) severe mitochondrial dysfunction is reported in the PD model and PD patients; 2) mitochondria-mediated damage plays an important role in inducing neuro-inflammation; 3) mortalin and/or mortalin interacting proteins appear to be affected in PD; 4) mortalin can attenuate the Lewy bodies and α-Syn-induced neuronal toxicity; 5) Parkin and PINK1 can act as mitochondrial protector. This evidence concerns the gene PRKN and Parkinson disease.