In addition, an Alzheimer's disease (AD) model was constructed in mouse neuronal cells, and it was found that overexpression of ARMC10 reduced the number of mitochondria in neuronal cells in the exercise state and promoted the occurrence of mitochondrial aggregation; at the same time, overexpression of ARMC10 rescued mitochondrial fragments, reduced β‐amyloid (Aβ)‐induced neuronal apoptosis and exerted neuroprotective effects.20 This evidence concerns the gene ARMC10 and Alzheimer disease.