The patient was a 70-year-old female who visited Beijing Hospital in 2014 for weakness, amaurosis and profuse sweating. The hemoglobin concentration was 63g/L (6.3g/dL). The white blood cell count was 6.49x109/L. The platelet count was 100x109/L. The laboratory chemistry profile showed total protein 110g/L, albumin 36g/L, calcium 2.32 mmol/L, creatinine 74 umol/L. The immunoglobulin profile showed IgA 80g/L, IgG 4.15g/L, IgM 0.04g/L. The serum and urine immunofixation electrophoresis demonstrated IgA-Kappa (IgA-kappa) monoclonal gammopathy and the beta2-microglobulin was 8.89mg/L. Bone marrow aspiration showed monotypic plasma cells accounted for 60%. The final diagnosis was IgA-kappa type multiple myeloma, International staging system (ISS) III and Durie-Salmon stage (D-S) IIIB. She had no significant medical history other than a myomectomy. She consecutively received six cycles of chemotherapy with different combinations of drugs, containing bortezomib, thalidomide, lenalidomide, ixazomib, cyclophosphamide, and dexamethasone. But this patient still suffered repeated disease progress due to drug intolerance. In November 2019, she was diagnosed with relapsed and refractory MM (r/rMM). Daratumumab was then initiated. After a transient improvement, the disease progressed again in May 2020, impelling bortezomib to be used again. In June 2020, the patient developed bilateral pleural effusion when the frequency of daratumumab was reduced (Figure 1A, June 8, 2020, chest Computerized Tomography (CT)). Diagnostic thoracentesis showed bloody effusion with features suggestive of an exudate (specific gravity 1.030, nucleated cells count 11,530/mm3, mononuclear cell 88%, total protein 36.7g/L, albumin 23.5g/L, lactate dehydrogenase (LDH) 463 U/L, ADA 40.1 U/L). Microbiological examination including fungus and mycobacterium tuberculosis did not reveal any pathogens, and the next-generation sequencing (NGS) technology disclosed no pathogen either. Cytological analysis and flow cytometry analysis revealed a large number of abnormal plasma cells. On June 9, 2020, we detected the cytokine profile in peripheral blood and right-sided pleural effusion using CBA technology and the results are listed in Table 1. Subsequently, consecutive thoracic drainage was performed in combination with Daratumumab, liposomal Adriamycin, Thalidomide and Dexamethasone (DATD). The right-sided pleural effusion then decreased after 1 week. On June 15, 2020, we detected the cytokine profile in right-sided pleural effusion second time and the results are listed in Table 1. Due to the DATD intolerance, the chemotherapy regimen was changed to pomalidomide and dexamethasone. The disease remained stable. In July 2020, patient ceased taking pomalidomide due to myelosuppression. As a result, the left-sided pleural effusion began to increase slowly (Figure 1B: July 15, 2020, chest CT). The patient developed dyspnea in August 2020 with chest CT (Figure 1C, August 17, 2020) signifying the obvious increase of left-sided pleural effusion. Again, a microbiological examination of left-sided effusion found no pathogens. Cytological analysis and flow cytometry analysis revealed a large number of abnormal plasma cells. On August 17, 2020, the cytokine profile in left-sided pleural effusion was detected by CBA technology, and the results are listed in Table 1. The chemotherapy of liposomal Adriamycin plus dexamethasone was chosen together with respiratory support, left-sided thoracic catheterization drainage and antibiotics therapy. However, after a temporary improvement, the patient's disease continuously progressed. Chest CT was examined in September (Figure 1D, September 3, 2020), disclosing ground-glass opacity and consolidation in the right lung, diffuse ground-glass opacity in the left lung, the progression of lesions in upper lobe and decrease of bilateral pleural effusion. The patient died of exacerbation of pulmonary infection and respiratory failure on September 8, 2020.