Chronic lymphocytic leukaemia (CLL) is the most common form of leukaemia in the western world within adults. It is a lymphoproliferative disorder involving progressive accumulation of mature CD19 + CD5 + B lymphocytes in the Peripheral Blood (PB), Bone Marrow (BM) and other lymphoid organs such as the Spleen (SP) and Lymph Nodes (LN). 1 The clinical features of CLL show high heterogeneity among patients; this variability could be explained by both intrinsic factors (e.g. genetics and epigenetics) and external stimuli. Despite the introduction of new effective targeted therapies such as BTK (e.g. ibrutinib, acalabrutinib) and BCL-2 (e.g. venetoclax) inhibitors, a majority of patients eventually relapse, so CLL still remains an incurable disease. 2,3 A major role in the development of the disease and the onset of drug resistance is played by the crosstalk between the malignant clone and the Tumour Microenvironment (TME). Malignant B cells recirculate between lymphoid organs and the bloodstream but while
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