To our knowledge, this is first demonstration that the interaction between CCN1 with α6β1, which is known to induce apoptosis or cellular senescence in fibroblasts to regulate the inflammatory response and control fibrosis during wound healing [11–13, 23], can be co-opted by ER-positive breast cancer cells to over-ride estrogen dependency and evade the growth-inhibitory effects of anti-estrogens (Figure 4A). Here, CCN1 is linked to breast carcinoma.