In addition, we also found that high-risk PRAD patients were associated with activated proliferation pathways, including the cell cycle, DNA duplication, and meiosis, which may be explained by the effect of EPHB1-GSK3B-SMAD3 signaling pathway activation on promoting tumor cell viability, invasion, and proliferative activity, macrophage M2 polarization, and inhibition of the expression of antiapoptotic proteins. This evidence concerns the gene GSK3B and prostate adenocarcinoma.