Moreover, FDCs are capable of sustaining CLL proliferation and survival by many other mechanisms, including BCR activation on CLL cells during the presentation of unprocessed antigens via complement receptors 1 (CR1/CD35) and 2 (CR2/CD21) and the expression of survival factors such as BAFF and a proliferation-inducing ligand (APRIL) and molecules involved in CAMDR, including VCAM-1 [39]. Here, BCR is linked to B-cell chronic lymphocytic leukemia.