However, since CD47 protects RBCs and platelets from destruction by myeloid cells, inhibiting this pathway may lead to adverse effects such as anemia173–176 and thrombocytopenia,177,178 which requires patients to receive a preceding low dose priming in the clinic.179,180 The Fc-FcγR interaction required for the anti-tumor activity of anti-CD47 mAbs is another contributor to these off-tumor adverse effects.181 Thus, the balance between effect and toxicity is crucial in CD47 drug development. The gene discussed is FCGR2A; the disease is neoplasm.