The potent inhibitory effects of Kindlin-2 deficiency on breast cancer progression and its role in regulation of AR (the current study) as well as other signaling pathways [36–47, 51, 55, 60–62, 67], together with the fact that Kindlin-2 is dispensable for normal mammary gland development (Supplementary Fig. 3), suggest that targeting the Kindlin-2 signaling pathway may provide a useful approach for therapeutic control of breast cancer progression and thus may help to improve the clinical outcome of human patients with breast cancer. This evidence concerns the gene AR and breast carcinoma.