Thioredoxin-interacting protein (TXNIP) is a key regulator of cellular metabolism and redox balance. TXNIP has also been implicated in regulating metabolic pathways during T cell activation and expansion. However, the specific impact of TXNIP on effector CD8⁺ T cell function and survival remains poorly defined. Single-cell RNA sequencing of CD8⁺ tumor-infiltrating lymphocytes across multiple murine tumor models and human cancers revealed that TXNIP expression was selectively enriched in the progenitor-exhausted T cell (Tpex) cluster compared with the terminally-exhausted T cell (Ttex) cluster, suggesting a close association between TXNIP and CD8⁺ T cell differentiation and function. Based on this observation, we employed antigen-specific TCR-transgenic CD8⁺ T cells to evaluate the role of TXNIP during the effector stage. Pharmacological inhibition of TXNIP in antigen-activated CD8⁺ T cells led to a marked increase in the cell surface expression of activation markers and effector molecules, while overall cell viability was largely preserved. In conclusion, TXNIP modulation differentially regulates effector CD8⁺ T cell function and survival, with inhibition enhancing effector activity while preserving viability. These findings identify TXNIP as a potential therapeutic target to enhance adoptive cell therapy.