This dual approach effectively decreased collagen deposition, increased CD8 + T cell infiltration, and suppressed PD-L1 expression in murine models of triple-negative breast cancer, surpassing that of targeting either receptor alone, highlighting a synergistic ECM reprogramming deriving from DDR2 ability to mediate collagen-cell interactions and ITGAV ability to sustain TGF-β1 activation. This evidence concerns the gene DDR2 and triple-negative breast carcinoma.