While claudin-1’s role as a proponent of cell migration, invasion and the EMT phenomenon is well documented in other cancers [38], in breast cancer there is evidence that claudin-1 may have a dual role, first as a target for one or more of the EMT pathway molecules such as β-catenin and Slug/Snail-1 [20], or secondly as an effector altering the expression of EMT-related molecules either by transcription factors’ activation such as slug and zeb1 or through modulation of the β-catenin/Tcf signaling pathway [16]. The gene discussed is SNAI2; the disease is cancer.