CD47 that is expressed on GBM surface could combine with the V-like domain at the NH2-terminal of SIRPα that is expressed on macrophages result in the phosphorylation of tyrosine residues in the immune-receptor tyrosine-based inhibition motifs (ITIMs), leading to the tyrosine phosphatase SHP1/SHP2’s activation, finally, prevent GBM from phagocytosis by macrophages [5]. The gene discussed is SIRPA; the disease is glioblastoma.