Combined with our research, pharmacological and genetic overexpression of PINK1 and Parkin can significantly alleviate neuronal apoptosis and death in prion disease, suggesting that mitochondrial dysfunction and bioenergy deficiency in prion disease may be alleviated by stimulating PINK1-parkin-mediated mitophagy, thereby fostering a healthy mitochondrial pool and ultimately significantly increasing neuronal activity. The gene discussed is PRKN; the disease is prion disease.