Although the precise origin of autoimmune response in the MG patients so far is not completely clear, it is believed that the genetic predisposition may influence the patients who have such a disorder.[3–6] Tumor necrosis factor α-induced protein 3 (TNFAIP3, also known as A20), which is a potent anti-inflammatory signaling molecule, can restrict and terminate the inflammatory responses through the modulation of ubiquination status of central components for the nuclear factor κB (NF-κB), interferon regulatory factor 3, and apoptosis signaling cascades.[7,8]. Here, NFKB1 is linked to myasthenia gravis.