TST (thiosulfate sulfurtransferase) is a mitochondrial enzyme that catalyzes sulfur transfer reactions, primarily functioning in cellular detoxification and metabolic regulation 1. The enzyme plays a crucial role in cyanide detoxification through thiosulfate-cyanide sulfurtransferase activity and participates in the formation of iron-sulfur complexes. TST operates through S-sulfhydration mechanisms, modifying target proteins to regulate their function 1. In diabetic kidney disease, TST deficiency leads to decreased S-sulfhydration of very long-chain specific acyl-CoA dehydrogenase, resulting in mitochondrial fatty acid oxidation dysfunction and exacerbated tubular injury 1. The enzyme shows reduced expression in metabolic diseases including diabetes and obesity, where its downregulation contributes to renal tubular impairment 1. Clinically, TST deficiency represents a potential therapeutic target for diabetic kidney disease, as sodium thiosulfate treatment or TST overexpression can mitigate renal tubular injury under high-glucose conditions 1. The enzyme's role in maintaining proper mitochondrial fatty acid metabolism makes it significant for understanding metabolic dysfunction in diabetes-related complications. Note: Several abstracts discuss 'TST' referring to different entities (thiostrepton drug, tumor-specific T cells, tuberculin skin test) rather than the TST gene, limiting available gene-specific functional information.