The present study demonstrated that the differential expression of HSD17B2, HSD17B3, SHBG, and SRD5A1 in patients with different PCa grades is suggestive of a dysregulated androgenic-signal-driven oncogenicity in patients with PCa, where intracellular signaling skewed towards a dominant SRD5A1/HSD17B3 at the expense of SHBG/HSD17B2 signaling drives enhanced cancerization, and may inform therapeutic decision making and management strategy for patients with PCa (Figure 1). Here, SHBG is linked to posterior cortical atrophy.