These effects may be of pathogenic relevance, since IL-6 may promote survival and proliferation of MCL cells in an autocrine/paracrine fashion, as recently demonstrated.[9] The potential relevance of interactions between MCL and the microenvironment has been further enforced through the demonstration that activating mutations of TLR2 triggered secretion of high levels of IL-6 in a subset of MCL. This evidence concerns the gene TLR2 and mantle cell lymphoma.