The nuclear accumulation of β-catenin was induced by Axl-activated Akt/GSK3β/β-catenin signaling, followed by a direct transcriptional increase in ZEB1, which in turn mediated DDR and doxorubicin resistance in breast cancer cells; these results suggest that the important function of Akt/GSK3β/β-catenin/ZEB1 signaling is downstream of Axl-mediated drug resistance [60]. Here, AXL is linked to breast cancer.