Collectively, these observations indicate that higher KL-6 expression in MCF-7 cells does not, by itself, determine invasive capacity; rather, invasion likely reflects the integrated effects of KL-6-dependent and KL-6-independent mechanisms, including epithelial-mesenchymal transition (EMT) status, NF-κB/Rac signaling, protease activity, and tumor-stroma interactions. Here, NFKB1 is linked to neoplasm.