These data, in the context of genomics of drug sensitivity in cancer, provide some proof of concept that re-reprogramming of testosterone metabolism via “SRD5A1 withdrawal” or “SHBG induction” is a workable therapeutic strategy for shutting down androgen-driven oncogenic signals, reversing cancer stem cell (CSC)-facilitated treatment resistance, and repressing the metastatic/recurrent phenotypes of patients with PCa. This evidence concerns the gene SHBG and posterior cortical atrophy.