Myasthenia gravis (MG) is a cell‐dependent autoimmune disease commonly associated with thymic pathology. Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT‐1) has been associated with gene regulation and alternative splicing. It has shown relationship with proliferation, apoptosis, migration, and invasion. In this study, we found that MALAT‐1 expression was downregulated in MG. The level of the miR‐338‐3p was increased in peripheral blood mononuclear cells from MG patients compared with those from control subjects. MALAT‐1 competed for binding to miR‐338‐3p with male‐specific lethal 2 (MSL2) in luciferase reporter assays. We confirmed the MALAT‐1‐miR‐338‐3p‐MSL2 interaction network in MG in vitro. Thus, MALAT‐1 directly induced MSL2 expression in MG by acting as a competing endogenous RNA for miR‐338‐3p, suggesting that it may serve as a therapeutic target for MG treatment. We confirmed the MALAT‐1‐miR‐338‐3p‐MSL2 interaction network in myasthenia gravis (MG) in vitro. Thus, metastasis‐associated lung adenocarcinoma transcript 1 (MALAT‐1) directly induced male‐specific lethal 2 (MSL2) expression in MG by acting as a competing endogenous RNA (ceRNA) for miR‐338‐3p, suggesting that it may serve as a therapeutic target for MG treatment.