This patient was a 61 years old Chinese male, who admitted into hospital for abdominal pain and discomfort in May of 2019. Ultrasound of abdomen showed enlarged lymph nodes and positron emission computed tomography and computed tomography (PET-CT) scan showed diffuse enlargement of lymph nodes (0.5-2.4cm) with high fluorine-18 fluorodeoxyglucose (FDG) intake (maximum standardized uptake value (SUVmax) 4.0-23.7) (Fig. 1A), However, he refused to receive any advanced examination except routinely follow-up. Eventually, he developed severe fatigue and jaundice in November of 2019 and laparoscopic biopsy of his abdominal mass revealed DLBCL which was positive for CD20, BCL2, CD10, MYC, BCL6 with Ki67 proliferation index 70%. Fluorescence in situ hybridization (FISH) detected BCL6 gene rearrangement of tumor cells while BCL2 and MYC rearrangement were negative. CT showed ground glass like nodules of lungs, pleura thickness, pleural effusion, abdominal mass surrounding head of pancreas and large ascites. His disease status was stage IV with B symptom according to Ann Arbor staging system. Fractioned R-CDOP regimen (rituximab, cyclophosphamide, pegylated liposomal doxorubicin, vincristine, prednisone) was given to him and his symptom and abdominal mass resolved quickly. Unfortunately, his mass appeared again before the second cycle, then second and third R-CDOP were given to him. Based on Lugano 2014 criteria, interim clinical response after three cycles was stable disease. Next generation sequence of his peripheral blood showed BCL2 amplification and TP53 mutation. Second line regimen R2 + GDP (rituximab, lenalidomide, gemcitabine, dexamethasone, and cisplatin) failed to improve his disease status and third line R2 + ibrutinib + reduced intensity ESHAP (etoposide, methylprednisolone, cytarabine, and cisplatin) transiently relieve his abdomen discomfort but jaundice appeared again after another course of R2 + ibrutinib without chemotherapy due to cytopenia (Fig. 1B). Since high expression of BCL2 protein and BCL2 amplification of his tumor cells, we determined to treat him with BCL2 inhibitor plus low intensity chemotherapy including vindesine and dexamethasone, with BCL2 inhibitor escalation from 100mg to 400mg in one week quickly. Surprisingly, ten days after treatment, no tumor lysis syndrome (TLS) was observed and physical examination found reduction of abdominal mass. Three weeks after BCL2 inhibitor therapy, PET-CT scan showed obvious reduction of FDG intake among these lesions (SUVmax 3.7) (Fig. 1C) with partial remission. To prolong duration of response, autologous peripheral T cells were apheresis collected and transduced with an apoptosis-inducible, safety-engineered lentivector CAR containing four intracellular signaling domains: CD19-scFv//CD28/CD137/CD27/CD3ζ-iCasp9. Lymphodepleting regimen consist of fludarabine 30mg/m2 and cyclophosphamide 500mg/m2 for 3 days was given before CAR T-cell infusion. The dose of CAR T-cells were 2.4×106/kg. He suffered from fever on day 5 and 6, not exceeding 38.2℃, and after excluding infection, grade 1 CRS was diagnosed. Ten days after infusion, physical examination showed disappearance of his abdominal mass, however, delayed pancytopenia appeared and lasted for more than two months (Fig. 2). Moreover, on 54th day of infusion, he complaint of high fever and short of breath, with low blood pressure and high C reactive protein (CRP). Ultrasound of his heart showed ejection fraction 66%. However, his symptom didn’t resolve by antibiotic therapy. On 57th day, his ferritin increased from 2340ng/ml on 55th day to 55577ng/ml with interleukin-6 (IL-6) from 277.8 pg/ml to 903 pg/ml, then dexamethasone 10mg q6h was given for a secondary severe CRS. 0n 58th day, his B-type natriuretic peptide (BNP) increased to more than 5000 pg/ml with cardiac troponin I (cTNI) 2499 pg/ml revealing acute cardiac injury (Fig. 3). However, he responded well to steroid, including rapid control of pyrexia, return to normal level of cardiac function and cardiac enzyme, which supported diagnosis of a secondary CRS. PET-CT of the third month demonstrated partial remission with obvious reduction of abdominal mass (Fig. 1D) and he is still in follow-up now.