Estrogen-dependent MCF-7 breast cancer cells, which naturally express very low levels of CCN1, were engineered to stably overexpress either wild-type CCN1 or the mutational derivatives D125A-CCN1, which exhibits a disrupted αvβ3-binding site through the D125A mutation, and TM-CCN1, which abrogates all the T1, H1, and H2 binding sites to α6β1 (Figure 1) [25–28]. The gene discussed is CCN1; the disease is breast carcinoma.