We report a patient who developed anti-LGI1 antibody-associated encephalitis during ongoing efgartigimod therapy despite reduced serum IgG levels, raising considerations regarding the mechanisms of central nervous system autoimmunity under FcRn inhibition.<h4>Methods</h4>A 72-year-old woman with thymoma-associated MG receiving efgartigimod was evaluated after presenting with rapidly progressive memory impairment. The gene discussed is LGI1; the disease is myasthenia gravis.