The therapeutic landscape for multiple myeloma has dramatically changed over the past decades and recent progress in the treatment options for multiple myeloma, in particular with the incorporation of anti-CD38 targeting mAbs into standard care regimens including proteasome inhibitors (PI) and immunomodulatory drugs (IMiD) has tremendously improved the prognosis of patients with multiple myeloma (1–3). The gene discussed is CD38; the disease is AL amyloidosis.