TIMM29 (translocase of inner mitochondrial membrane 29) is a metazoan-specific subunit of the TIM22 complex, a multisubunit translocase embedded in the mitochondrial inner membrane 1. The primary function of TIMM29 is to facilitate the import and insertion of multi-pass transmembrane carrier proteins into the mitochondrial inner membrane, using the membrane potential as a driving force 1. TIMM29 is essential for TIM22 complex stability and assembly, and mediates physical contact between the TIM22 and TOM (outer membrane) complexes to enable transport of hydrophobic substrates across the intermembrane space 1. Functionally, TIMM29 supports iron-sulfur cluster biogenesis by facilitating mitochondrial iron uptake through its role in stabilizing iron transporter proteins on mitochondria, thereby promoting cell proliferation 2. Disease relevance is substantial: biallelic TIMM29 variants cause Sengers syndrome, characterized by congenital cataracts, hypertrophic cardiomyopathy, skeletal myopathy, and lactic acidosis, accompanied by combined respiratory chain deficiency and abnormal mitochondrial accumulation 3. Clinically, TIMM29 also modulates hepatitis B virus replication through interactions with the HBV preS1 protein; its expression suppresses HBV amplification by upregulating antiviral factors like SRSF1 4. These findings establish TIMM29 as critical for both mitochondrial biogenesis and innate antiviral defense.