Moreover, in prostate cancer ACKR1 expressed by vascular endothelial cells interacted with tetraspanin KAI1 (CD82) on tumor cells, leading to decreased DNA synthesis and induction of tumor cell senescence (195); in parallel, it was found that melanoma-expressed KAI interacted with endothelial cell-expressed ACKR1 preventing CXCL8-inudced gap formation in endothelial cells and leading to tumor cell senescence (197). This evidence concerns the gene CD82 and prostate cancer.