The effect of FOXA1 on AR signaling is dichotomy in that increasing FOXA1 activity induces non-selective opening of closed chromatin, inducing the binding of AR to ARE half-sites at expense of gens with canonical ARE that promote cancer progression; in contrast, FOXA1 inhibition reprogrammed AR binding to AREs, leading to overexpression of some androgen-responsive genes, thus promoting CRPC cell growth [648]. This evidence concerns the gene AR and cancer.