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A 66-year-old man was diagnosed with chronic lymphocytic leukaemia (CLL) in November 2014. At diagnosis, his lymphocyte count was 169.66×10 9/L (table 1). The fluorescent in situ hybridisation (FISH) panel revealed 13q deletion, but there was no evidence of 17p deletion, 11q deletion or t (11;14). He then received four cycles of bendamustine and rituximab, and at the end of the treatment complete blood count showed a lymphocyte count of 1.01×109/L (table 1), and an interval bone marrow biopsy showed only small lymphoid aggregate suggestive of partial response.1 In June 2017, his lymphocyte count was found to be elevated at 14.5×109/L (table 1). An immunophenotypic analysis of the peripheral blood demonstrated approximately 78% lymphocytes and 0.5% mature CD14-positive monocytes. A predominant monoclonal B cell population was identified, comprising approximately 85% of lymphocytes and 67% of the processed specimen. It was positive for CD5, CD19, CD20, CD23, CD45, human Leukocyte Antigen – antigen D Related (HLA-DR) and surface kappa light chain, and negative for CD10, CD22, CD38 and FMC7. The remainder of lymphocytes included approximately 7% T cells with a CD4/CD8 ratio of 1.3. In summary, a predominant partially CD5-positive, kappa-restricted monoclonal B cell population was identified, immunophenotypically similar to that identified in previous bone marrow biopsy except that partial CD5 expression was identified. The FISH panel revealed 13q deletion with no evidence of 17p deletion, 11q deletion or t(11;14), similar to the results at the time of diagnosis. The patient was kept on surveillance as there were no cytopaenias and no other indication of treatment. Three months later he presented to the emergency department with haematuria. CT of the abdomen/pelvis showed a mass in the urinary bladder. CT urography showed an intravesical mass in the left wall bladder with bladder wall infiltration, and additional intraluminal soft tissue mass projecting in and about the region of the ureteral entry through the ureterovesicular junction at the bladder trigone (figure 1). Transurethral resection of bladder tumour was performed, and the mass was 2.4×1.0×0.5 cm in size. Histopathology showed low-grade lymphoproliferative disorder characterised by a diffuse proliferation of small mature lymphocytes associated with a few large lymphoid cells and rare eosinophils (figure 2). Immunohistochemical analysis showed small neoplastic lymphocytes positive for CD20, CD23, CD79a, CD5, BCL2 and BCL6 with weak intensity, and CD43. The neoplasm showed a Ki-67 proliferation fraction of approximately 20%. A few reactive plasma cells exhibited polyclonal staining pattern for kappa and lambda immunoglobulin light chains. Rare plasma cells were positive for CD138. CD3 highlighted a small population of T cells. The above findings were consistent with CLL/small lymphocytic lymphoma. A positron emission tomography (PET)-CT was obtained. The PET part was unremarkable, while the CT showed an increased number of small lymph nodes in the mesentery as well as in the upper retroperitoneum. CLL in the urinary bladder is a rare manifestation.