TIMM17B (translocase of inner mitochondrial membrane 17B) is an essential component of the TIM23 protein translocase complex, which mediates translocation of presequence-containing proteins across the mitochondrial inner membrane into the matrix 1. Human cells express two TIMM17 paralogs—TIMM17A and TIMM17B—that form structurally similar TIM23 variants with comparable translocation mechanisms to yeast homologs 1. The TIM23 complex requires both the electrochemical potential across the inner membrane and ATP for function 2. TIMM17B stability is regulated by the prohibitin complex and OCIAD1, which protects the TIMM17B-containing TIM23 variant from YME1L-mediated degradation 3. Clinically, TIMM17B downregulation is associated with heart failure in ischemic and dilated cardiomyopathy patients, indicating defective mitochondrial quality control 4. Conversely, elevated TIMM17B expression correlates with worse prognosis in basal breast cancer, is negatively associated with immune infiltration, and links to drug resistance and ferroptosis dysregulation 5. TIMM17B downregulation appears in degenerative ascending thoracic aortic aneurysm tissues alongside mitochondrial dysfunction 6. Genetic variants in the TIMM17B locus associate with primary biliary cholangitis susceptibility in East Asian populations 7. These findings suggest TIMM17B serves dual roles: its loss impairs cardioprotection, while its elevation promotes cancer progression.