Meanwhile, EPHB1 protein interaction with GSK3B protein enhanced the phosphorylation levels of GSK3B and SMAD3, while the knockdown of GSK3B reduced the phosphorylation of SMAD3. Based on these findings, it can be concluded that EPHB1 played a crucial role in activating the EPHB1-GSK3B-SMAD3 pathway to support PRAD progression. Here, EPHB1 is linked to prostate adenocarcinoma.