Given the crucial role of AR in breast cancer progression [9–12] and the fact that AR is a substrate of Src [13, 14, 16, 19, 20], to which Kindlin-2 binds [48], we decided to focus on the role and mechanism of Kindlin-2-mediated regulation of AR tyrosine phosphorylation, signaling and breast cancer progression in the current study. This evidence concerns the gene FERMT2 and breast carcinoma.