Specifically speaking, these mechanisms include AR overexpression [27] or coactivator overexpression [28] that sensitizes AR to reduced androgen level physiologically, including point mutations that may lead to the promiscuous activation of AR by nonandrogenic steroids with the relative abundance; the AR being activated/sensitized through the protein phosphorylation [29]; and the androgen de novo production on its own of the tumor [6]. Here, AR is linked to neoplasm.