Furthermore, contextualized within the genomics of cancer drug sensitivity, we also provided 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 (Figure 5). This evidence concerns the gene SHBG and posterior cortical atrophy.