Similarly, treatment with anti-CD20 mAbs (ofatumumab, obinutuzumab, and rituximab) for B cell malignancies as well as the anti-CD52 mAb alemtuzumab for B-cell chronic lymphocytic leukemia or the anti-CD38 mAb daratumumab for multiple myeloma resulted in no to low incidences of ADA development, with no observed ADA-related effects on treatment safety and efficacy [21, 54, 55]. The gene discussed is ADA; the disease is AL amyloidosis.