Kang et al. (2018) developed a cell-penetrating artificial mitochondria-targeting peptide (CAMP), which could conjugate the antioxidant protein human metallothionein 1A (hMT1A) to form CAMP-hMT1A successfully localized to the mitochondria. CAMP-hMT1A restored mitochondrial activity, tyrosine hydroxylase production, and inhibited ROS release after treating a cell Parkinson’s disease model. Furthermore, CAMP-hMT1A injected into the brain of the PD mouse model protected dopaminergic neuronal degeneration and movement impairment (Dinca et al., 2016). This evidence concerns the gene MT1A and Parkinson disease.