While these data might suggest that binding to α6β1 is largely responsible for the capacity of CCN1 to regulate ERα transcriptional activity in an endocrine-resistant phenotype, future studies will be needed to clarify whether a direct interaction between CCN1 and ERα, which might be disrupted in the case of TM-CCN1, is required for the activation of estrogen/tamoxifen-responsive transcription by CCN1 in endocrine-resistant breast cancer cells (Figure 4). This evidence concerns the gene CCN1 and breast cancer.