ACTR10 is a dynactin complex component essential for retrograde mitochondrial transport along axonal microtubules 1. This actin-related protein mediates the interaction between dynactin and mitochondria, enabling dynein-powered movement toward the cell body 1. Loss-of-function mutations in actr10 cause abnormal axon morphology and impaired mitochondrial retrograde transport, with genetic evidence implicating Drp1 as a functional partner 1. Retrograde mitochondrial transport via ACTR10 is critical for maintaining healthy mitochondrial distribution in neurons and supporting motor axon function 2. ACTR10 dysfunction has emerged as a disease biomarker. It was identified as a key hub gene in Alzheimer's disease immune-related pathways 3 and among five critical vesicle trafficking-related biomarkers in AD pathogenesis 4. In prion diseases, ACTR10 perturbation significantly affects prion propagation and clearance 5, with potential implications for broader neurodegeneration involving protein aggregates. In hepatocellular carcinoma, ACTR10 upregulation promotes tumor progression and mediates tyrosine kinase inhibitor resistance through altered RNA splicing, mRNA processing, and nucleocytoplasmic transport 6. ACTR10 also serves as a prognostic marker in primary central nervous system lymphoma 7. These findings establish ACTR10 as a pleiotropic regulator linking intracellular transport dysfunction to neurodegenerative and malignant disease pathogenesis.