FERMT2 and breast carcinoma: 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.