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. The gene discussed is SRC; the disease is breast carcinoma.