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. Here, SMAD3 is linked to neoplasm.