SNPH (syntaphilin) is a mitochondrial docking protein that functions as a static anchor inhibiting mitochondrial movement and dynamics 1. At the molecular level, SNPH anchors mitochondria to the microtubule cytoskeleton through tubulin binding, preventing their accumulation at the cell cortex 2. This anchoring function is regulated by non-degradative ubiquitination by the E3 ligase CHIP at Lys111 and Lys153; disrupting ubiquitination increases mitochondrial motility and activates dynamin-related protein-1 (Drp1)-dependent fission dynamics 2. In disease contexts, SNPH abnormalities have emerged as clinically relevant. Plasma neuronal extracellular vesicles from major depressive disorder patients show significantly reduced SNPH levels, which normalize with successful SSRI treatment 3. In esophageal cancer, SNPH downregulation facilitates radioresistance by promoting sparse mitochondrial distribution and reducing oxidative damage; SNPH re-expression promotes radiosensitization and serves as an independent prognostic factor 4. In Alzheimer's disease, APP and its derived fragments alter SNPH expression, impairing mitochondrial-transport protein colocalization and contributing to mitochondrial transport defects 5. Therapeutically, SNPH inactivation could enhance axonal mitochondrial transport to improve spinal cord injury recovery 1, positioning SNPH as both a biomarker and potential therapeutic target across neurological and oncological diseases.