However, these genes are also enriched for binding of oncogenes like FOXA1 [50], and recent work has suggested that in late-stage disease, these sites may be more tumor-promoting, in that they can be occupied by an AR monomer during androgen deprivation [51], and co-factors can drive oncogenic activity off of the sAREs [52], with cAREs actually being more tumor suppressive. The gene discussed is FOXA1; the disease is neoplasm.