Several mechanisms may contribute to the loss of B cell tolerance in peripheral lymph nodes in the context of tumor ectopic expressions or potential viral infections, particularly by inducing B cell-intrinsic Toll-like receptor (TLR) signal together with B cell receptor (BCR) ligation, or activating T helper (Th) cell with same antigen stimulation, thereby leading to consecutive B cell clonal expansion, class switch, affinity maturation and NSAbs production [24, 27, 28]. This evidence concerns the gene BCR and viral infectious disease.