TRABD (TraB domain containing) is a mitochondrial outer membrane protein that regulates mitochondrial dynamics and cellular homeostasis. Functionally, TRABD promotes mitochondrial fusion and clustering by forming complexes with MFN2, MIGA2, and PLD6 1, and interacts with the TOM complex to facilitate mitochondrial protein import 2. TRABD depletion impairs mitochondrial respiration, ATP production, and increases reactive oxygen species (ROS) levels, while also disrupting mitochondrial dynamics and mitophagy possibly through PGAM5 interactions 3. In disease contexts, elevated TRABD expression correlates with tau pathology and neurodegeneration in Alzheimer's disease 14. TRABD overexpression increases ROS and enhances tau toxicity in aging organisms, contributing to age-related neurodegeneration 1. Conversely, in triple-negative breast cancer, TRABD upregulation via the HLA-F-AS1/miR-541-3p axis promotes cell proliferation and stemness 5, while TRABD suppression through ZC3H13-mediated ferroptosis reduces doxorubicin resistance 6. Additionally, TRABD methylation alterations are associated with EBV-positive gastric cancer development 7. In acute kidney injury, TRABD knockout exacerbates ischemia-reperfusion-induced renal tubular damage by promoting mitochondrial fragmentation 3. These findings establish TRABD as a critical regulator of mitochondrial homeostasis with distinct roles in age-related neurodegeneration and cancer pathogenesis.