A key difference in IBC and non-IBC is the ubiquitous presence of E-cadherin in primary tumors, tumor emboli or clusters in the lymphatic system, and metastases,64, 65 a presence which might appear paradoxical given the established role of E-cadherin as a metastasis suppressor in a variety of cancers.66 On the contrary, E-cadherin appears to augment the invasion of SUM 149 cells, an IBC cell line, by increasing the levels of matrix metalloprotease enzymes such as MMP-1 and MMP-9,66 suggesting that E-cadherin can promote IBC progression. This evidence concerns the gene MMP1 and inflammatory breast carcinoma.