Based on these findings, we propose a model (Fig. 7) in which Kindlin-2 acts as a key scaffolding protein to facilitate the association of Src with AR and consequently promote AR Tyr-534 phosphorylation and downstream signaling in response to extracellular stimuli such as EGF, resulting in increased cell proliferation, migration and breast cancer progression. This evidence concerns the gene FERMT2 and breast cancer.