Its activation through the SEMA4D/PlexinB1 axis results in the increased proliferation of acute myeloid leukemia cells, the increased metastasis and growth of cancer cells in osteosarcoma, bladder cancer, pancreatic cancer, prostate cancer, and can even reduce the effectiveness of nivolumab in melanoma therapy [55,76,77]. This evidence concerns the gene PLXNB1 and prostate cancer.