Myeloid checkpoint inhibition at the phagocytosis axis is mechanistically justified: the CD47–SIRPα pathway suppresses macrophage effector function across solid tumors, yet in glioma, CD47 blockade shows limited activity as monotherapy and demonstrates improved phagocytic and antitumor effects when combined with genotoxic stressors, supporting rational combinations with standard therapy or opsonizing antibodies. Here, CD47 is linked to glioma.