EMT-regulating factors have been linked to increased mammosphere formation and tumor-initiating cells [30], and loss of E-cadherin is a hallmark of EMT that correlates with promotion of invasion and metastasis [31], but because E-cadherin is overexpressed in this highly metastatic disease and maintained with MSC promotion of IBC features, our in vivo results validate the disconnect between the EMT-tumor-initiating cell axis and metastasis in IBC. The gene discussed is CDH1; the disease is neoplasm.