In the latter study, the ability to inhibit B lymphopoiesis required interactions between multiple myeloma (MM) cells, a PC-derived neoplasm, and stromal cells which led to increased expression of CCL3 (macrophage inflammatory protein-one alpha, MIP-1α) and CCL4 (macrophage inflammatory protein-one beta, MIP-1β) by stromal cells as well as increased expression of TGFB1 (transforming growth factor-beta one, TGF-β1) by both PCs and stromal cells (39). The gene discussed is CCL3; the disease is AL amyloidosis.