MG secondary to COVID-19 vaccination; This is a literature report.  A 46-year-old female patient received BNT162b2 (BNT162B2), as dose 1, single (Batch/Lot number: unknown) for covid-19 immunisation. The patient's family history included: "multiple sclerosis" (unspecified if ongoing). The patient's concomitant medications were not reported. The following information was reported: MYASTHENIA GRAVIS (hospitalization, medically significant, life threatening), 5 days after the suspect product(s) administration, outcome "unknown", described as "MG secondary to COVID-19 vaccination". The patient underwent the following laboratory tests and procedures: Electromyogram: showed 60-70% electrical decrement; NIF: -36 mmHg; mid -30, notes: at home averaging mid; Workup: unremarkable; Exam: showed bilateral ptosis (improvement with the ice, notes: pack test), dysarthria, weakness worst in proximal bilateral lower extremities and symmetric hyperreflexia. Therapeutic measures were taken as a result of myasthenia gravis.  Clinical course: INTRODUCTION: Acute MG exacerbations have been attributable to infections and medications. This has surged during the COVID-19 pandemic especially with medications like hydroxychloroquine and azithromycin initially used to treat acute infections. We present a case of new onset MG secondary to COVID-19 vaccination. DESCRIPTION: A 46 year old with a family history of multiple sclerosis presented with 4 months of progressive lower extremity weakness, starting five days after her initial BNT162b2 COVID-19 vaccine. She had difficulty rising from a seated position and raising her arms above her head associated with blurry vision. Exam showed bilateral ptosis (improvement with the ice pack test), dysarthria, weakness worst in proximal bilateral lower extremities and symmetric hyperreflexia. Workup was unremarkable. Pyridostigmine was initiated with improvement. Two months later, she was admitted to the ICU for acute progressive fatigability and shortness of breath concerning for myasthenic crisis. Electromyography/repetitive nerve stimulation of the ulnar nerve showed 60-70% electrical decrement. ABG was stable, but NIF was -36 mmHg. She underwent therapeutic plasma exchange (PLEX). She approached her baseline strength and was discharged on prednisone and mycophenolate mofetil. Two weeks later, she was again admitted with myasthenic crisis with daily NIF at home averaging mid -30s mmHg. She underwent PLEX with significant improvement and was initiated on biweekly PLEX as an outpatient. DISCUSSION: While vaccine-induced flares or onset of autoimmune disease have been described in the literature, new diagnosis of MG following vaccination is rare, limited to 1 to 3 case reports. No case presented after the first dose like our patient. One study on COVID-19 vaccination in patients with existing MG showed that the symptoms of MG did worsen after recombinant subunit vaccination. We query if the COVID vaccine induced a similar mechanism like cytokine storm which hyperstimulated the immune system to a point that broke immunologic self-tolerance. Our patient may have had low titers of pre-existing self-antigen to the AChR that were released upon administration of the BNT162b2 COVID-19 vaccine. However, this vaccine effect may represent a correlation; further studies are needed to infer causality.; Sender's Comments: As per the available information the causality of the event myasthenia gravis with the suspect can not be ruled out completely. The impact of this report on the benefit/risk profile of the Pfizer product is evaluated as part of Pfizer procedures for safety evaluation, including the review and analysis of aggregate data for adverse events. Any safety concern identified as part of this review, as well as any appropriate action in response, will be promptly notified to regulatory authorities, Ethics Committees, and Investigators, as appropriate.