TKT (transketolase) is a key metabolic enzyme that catalyzes the transfer of two-carbon ketol groups in the pentose phosphate pathway (PPP), specifically in the non-oxidative branch, using thiamine pyrophosphate as a cofactor 1. The enzyme plays critical roles in immune regulation, particularly in regulatory T cell (Treg) function, where TKT deletion causes fatal autoimmune disease by impairing Treg suppressive capability through metabolic disruption and DNA hypermethylation 1. In cancer contexts, TKT exhibits complex roles: it promotes metabolic dysfunction-associated fatty liver disease (MAFLD) by limiting inosine-induced mitochondrial activity when hyperinsulinemia increases TKT expression 2, and contributes to chemoresistance in urothelial cancer through metabolic reprogramming that enhances pyrimidine biosynthesis 3. TKT is also involved in hepatocellular carcinoma (HCC) pathogenesis, where it can be regulated by crotonylation to suppress tumor progression 4 and serves as a potential prognostic biomarker when overexpressed in both blood and tumor tissues 5. The enzyme's dysfunction is associated with autoimmune disorders, where TKT levels are frequently downregulated in Treg cells of affected individuals 1, highlighting its clinical significance in both metabolic diseases and immune regulation.