TNFAIP3 and myasthenia gravis: A20 is known as a potent inhibitor of NF-κB signaling pathway that may take an effort in the treatment.[7,8] On the other hand, although patients’ cells show increased expression of NF-κB-mediated proinflammatory cytokines, the TNFAIP3 mutant truncated proteins are likely to act by haplosufficiency since they do not exert a dominant-negative effect in overexpression experiment.[30] The current observations in our study may offer an opportunity to well understand the mechanisms of MG development and furthermore take proper medical actions to the MG treatments with different clinical features.