Because D125A does not impair the binding of CCN1 to α6β1, but fully prevents αvβ3-mediated intracellular signaling including induction of MAPK––which was previously demonstrated to drive chemoresistance in breast cancer cells [30]–CCN1-driven activation of MAPK appears to be dispensable for CCN1-driven endocrine resistance in breast cancer. This evidence concerns the gene CCN1 and breast carcinoma.