In our previous study, we revealed that ATAD3A is a key suppressor of Pink1‐mediated mitophagy.[24] Mutations or excess oligomerization of ATAD3A leads to mitochondrial dysfunction, which is closely associated with age‐related neurological symptoms, such as Huntington's disease and Alzheimer's disease.[26, 27, 48] However, the role of ATAD3A in cellular senescence and aging remains unclear. The gene discussed is PINK1; the disease is juvenile Huntington disease.