The C4-2 cells were treated with rCCL5, and the proteasome inhibitor MG132 or vehicle, and results revealed that MG132 blocked the CCL5-increased HIF2α expression (Figure 4b), suggesting that the CCL5 secreted by BM-MSCs may affect the protein stability of HIF2α in PCa cells. This evidence concerns the gene CCL5 and posterior cortical atrophy.