Of importance, previous studies using syngeneic prostate tumor models in CD47 deficient mice showed that inhibition of CD47 might have opposite consequences for tumor growth depending on the target cells: CD47/TSP-1 inhibition in tumor stromal ECs induces angiogenesis and tumor progression, and decreased TSP1 production in tumors from CD47 deficient mice reduced macrophage recruitments, whereas blocking the binding of CD47 on tumor cells with SIRPα on macrophages and DCs might, in contrast, induce an antitumor immune response and reduce tumor growth [94]. This evidence concerns the gene CD47 and neoplasm.