Model of cell growth–promoting effects of TLR ligands on malignant B cells. Recurrent bacterial or viral infections, or endogenous TLR ligands released by cellular stress (eg, collagen, fibronectin, heparin sulfate, heat-shock proteins) could favor the expansion of TLR-expressing malignant B-cell clones over those that have not acquired or retained TLR expression. TLR ligands would then promote cell growth and/or escape from immune surveillance.