Overexpression of SLC12A8 in normal breast epithelial cells recapitulated the exhausted T-cell phenotype, and TLR2 agonist treatment mimicked SLC12A8 effects.<h4>Conclusion</h4>SLC12A8 promotes immune evasion and metastasis in Luminal B breast cancer by inducing CD8<sup>+</sup> T-cell exhaustion via activation of the TLR signaling pathway, suggesting its potential as a prognostic biomarker and therapeutic target. This evidence concerns the gene TLR2 and breast carcinoma.