BCL2 and myasthenia gravis: EBV dysregulation of the host B cell system can lead to abnormal B cell survival and breakdown of B cell tolerance through mechanisms that involve: a) LMP1 and LMP2A expression, which are able to mimic activated CD40 and B cell receptor signaling [20]; b) induction of the anti-apoptotic protein Bcl-2 [52], known to be overexpressed in MG-associated thymomas [53]; c) synthesis of the B cell growth factor BAFF [54], known to be increased in serum and thymus of MG patients [55, 56]; and d) hypersensitivity to TLR stimulation [57].