It has been reported that Eya2 is required to mediate the prometastatic functions of Six1 via the induction of TGF-β signaling, epithelial-mesenchymal transition, and cancer stem cell properties [15]; EYA and SIX1 are often co-overexpressed in tumors, and the SIX1-EYA2 interaction has been shown to be critical for metastasis in a breast cancer model [12, 15, 45]. Here, EYA2 is linked to breast cancer.