In breast cancer, the intratumoral administration of the β-glucan curdlan, a ligand of dectin-1, reprograms tumor-infiltrating DC, favoring the generation of Th1 cells with a higher proportion of CD8+CD103+ T cells in tumors; this effect is abolished by the neutralization of TGF-β or inhibition of αvβ8 integrin (90). This evidence concerns the gene CD8A and breast cancer.