Acute Inflammatory Demyelinating Neuropathy; Guillain-Barre syndrome; This is a literature report.  Herein, we report a case of acute inflammatory demyelinating polyneuropathy (AIDP), the most common subtype of Guillain-Barre syndrome (GBS), following initial dose of mRNA COVID-19 vaccine in an adult LTR. PATIENT CASE A 65-year-old (patient race: redacted) male with cryptogenic cirrhosis underwent an uncomplicated deceased donor liver transplant in June 2020. In February 2021, he was hospitalized for subacute lower extremity weakness and paresthesia ascending to bilateral hands over 4 days. He denied fever, cough, diarrhea, rash, sick contacts, surgery, or trauma. He had received his first dose of the Pfizer-BioNTech COVID-19 vaccine two days prior to symptom onset. Pertinent medications included cyclosporine 75mg twice daily. Medical history was notable for coronary artery disease, diabetes mellitus, and hyperlipidemia. Neurological examination on admission showed bilateral lower extremity weakness, hyporeflexia and loss of pinprick sensation. He could only stand with support and required assistance for ambulation. By hospital day 3, the patient developed bilateral cranial nerve 7 palsies. He had extensive serum and infectious studies (White blood cells 3,500/uL (L) mild monocytosis (17%) ,Platelets 89,000/uL (L),Aspartate transaminase 149 IU/L (H),Alanine aminotransferase 294 IU/L (H) ,Alkaline phosphatase 233 IU/L (H), Total bilirubin 2.1 mg/dL (H),Westergren RBC sedimentation rate 20 mm,C-reactive protein 1 mg/dL,SPEP with few tiny oligoclonal bands in gamma region,Vitamin B12 884 pg/mL,IgA 214 mg/dL, IgM 71 mg/dL, IgG 1,194 mg/dL,Thyroid stimulating hormone 1.83 mIU/L,Paraneoplastic autoantibody panel negative,Chromogranin-A 403 ng/mL (ULN <93 ng/mL),Carcinoembryonic antigen 36 ng/mL (ULN <3 ng/mL, SARS-CoV-2 negative by nasopharyngeal swab PCR,Human immunodeficiency virus negative ,Epstein-Barr virus negative ,Cytomegalovirus negative ,Fungal cultures negative,Aerobic cultures negative,Rapid plasma reagin non-reactive,QuantiFERON-TB-Gold negative,Blood culture negative,Gastrointestinal pathogen panel stool PCR negative,Urine culture,Cerebral spinal fluid studies,Red blood cells 2 cells/cmm,White blood cells 1 cell/cmm,Protein 107 mg/dL (H),Glucose 87 mg/dL (H),HSV DNA by PCR negative,Cryptococcus Ag negative ,Acid-fast bacteria culture negative ,Flow cytometry negative for atypical or malignant cells,Cytology negative for carcinoma). Brain and spine MRI were normal. Cerebrospinal fluid showed elevated protein without pleocytosis. Electromyography (EMG) demonstrated prolongation of lower extremity f-waves and reduced recruitment of voluntary motor units without active denervation. He was diagnosed clinically and electrodiagnostically with Acute Inflammatory Demyelinating Neuropathy (AIDP) and treated with intravenous immunoglobulin (IVIG). Notably, his liver enzymes were newly elevated .Liver MRI showed innumerable new bilobar lesions. Liver biopsy demonstrated high grade neuroendocrine tumor of unclear origin plus mild acute rejection in his graft prompting initiation of prednisone. The patient exhibited good response to IVIG including improvement of facial palsies and ambulation. After 2 weeks in rehabilitation, he could walk independently (Table 2). Several etiologies were considered as inciting trigger for this patient's GBS. Infectious etiology was considered given his immunocompromised state, but extensive workup was negative . A rare paraneoplastic-associated GBS was also considered but deemed unlikely given negative serology plus improvement with IVIG alone prior to any treatment of his malignancy. Ultimately, his presentation including temporal association of symptoms and progression appeared most consistent with post-COVID-19- vaccination GBS. With respect to timing of vaccination, our patient received COVID-19 vaccination 8 months after transplant so his baseline immunosuppression would less likely inhibit immunogenicity. In conclusion, our report describes a strong temporal relationship between COVID-19 vaccination and onset of neurological symptoms consistent with post-vaccination GBS. An extensive medical evaluation failed to demonstrate any infectious, malignant, or alternative precipitant. We recognize that the patient's GBS following COVID-19 vaccination is strictly correlative, and appreciate the very real challenges of defining causality of vaccination with onset of GBS.9,10 However, we feel reporting this potential association is important given current gaps in understanding of COVID-19 vaccine safety among LTR. It is also important to note the patient demonstrated good response to standard GBS treatment once the diagnosis was established. Since the overall clinical benefit gained from COVID-19 vaccination outweighs the risk of rare adverse events like post-vaccination GBS, we recommend all LTR undergo COVID-19 vaccination. Finally, transplant providers should report all potential vaccine-related adverse events to the VAERS registry.; Sender's Comments: As there is limited information in the case provided, the causal association between the events Acute Inflammatory Demyelinating Neuropathy and Guillain-Barre syndrome and the suspect drug bnt162be cannot be excluded. 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.