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depleted of both of them (Figure C). NNK-SMZL expressed significantly higher levels of genes belonging to NOTCH2 pathway and of genes that are activated by non-canonical NF-κB transcription factors. Conversely, DMT-SMZL had a signature of TP53 and apoptosis impairment (Figure D). Digital cytometry and in situ profiling segregated two basic types of SMZL immune microenvironment termed inflamed SMZL (50% of cases, associated with inflammatory cells and immune checkpoint activation) and noninflamed SMZL (50% of cases) (Figure E and F). The combination of molecular and phenotypic profiling allowed to sort out a high risk clinical subset of patients whose tumor was characterized by having both NNK genotype and ''inflamed'' microenvironment (Figure G). Conclusions: Our study highlights the complexity of SMZL. The molecular framework provides an evolving understanding of the pathogenesis of SMZL, and can be regarded as a building block for further refining the classification of B-cell tumors of the spleen, and for aiding the development of rationally targeted treatments.

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