In fact, Miller et al.46have ever found both aging and genetic susceptibility were required for the occurrence of disease phenotypes, such as loss of tyrosine hydroxylase (TH) expression and enlarged mitochondria or Lewy‐body‐precursor inclusions using a premature aging model by expressing progerin, a truncated form of lamin A. Because aging plays an essential role in the pathogenesis of PD, anti‐aging therapies would provide new opportunities for the development of disease‐modifying treatments for PD.47, 48. This evidence concerns the gene TH and Parkinson disease.