This literature marketed report has been received from the authors of a published literature article, titled as stated above, containing retrospectively measured using 2 matched cohorts and refers to 39 patients of unknown gender with median age 74.3 (61.3-95.6) years without a history of immunosuppression who were seen by their primary care provider at some point in the years 2000 through 2015. There was no information about the patients' concurrent conditions, concomitant therapies, drug reactions, allergies or medical history provided. The patients did not have history of HIV/AIDS, leukemia, lymphoma, myeloma, myelodysplastic syndrome and did not have history of any prescription of the immunomodulating druganti-IL6, B-cell blockade, calcineurin inhibitors, costimulation blockade, disease-modifying antirheumatic drugs, interleukin-1 inhibitors, interleukin-17 inhibitors, monoclonal TNF-alpha antibody, mammalian target of rapamycin (mTOR) inhibitors, tumor necrosis factor (TNF) inhibitors, chemotherapy, and 2 or more prescriptions of glucocorticoids within the past year.  On unknown dates, the patients were vaccinated with live attenuated herpes zoster vaccine (manufacturer unknown) (formulation, strength, dose, route of administration, lot # and expiration date were not reported) for prophylaxis.  On unknown dates, the patients developed giant cell arteritis (GCA). 16 patients (41%) were diagnosed via positive biopsy and 23 (59%) were diagnosed by nonpathological College of Rheumatology clinical criteria. The median time from live attenuated herpes zoster (ZVL) vaccination to a diagnosis of GCA was a median (range) of 37.7 (4.9104.3) months, with peaks around 15 months and 45 months The outcome of the event was unknown.  According to authors, matched comparison of ZVL vs non-ZVL patients showed that vaccinated patients had a significantly higher incidence of GCA. This association may potentially be attributed to (1) subacute or persistent arterial wall infection with ZVL, (2) a ZVL vaccine-driven cellular immune response to VZV already present in the arterial walls, or (3) a non-viralspecific autoimmune reaction triggered by ZVL. Using proportional hazards regression models of time to GCA by combination of both diagnostic case criteria, ZVL vaccination was associated with an increased risk of GCA diagnosis (hazard ratio [HR], 2.20; 95% CI, 1.503.24; P < .0001). In the more specific, biopsy-confirmed subset of GCA cases, ZVL receipt remained a significant risk factor for GCA (HR, 2.70; 95% CI, 1.484.95; P = .004). The authors performed a secondary analysis incorporating only those patients from the original matched cohort whose follow-up period included the year 2008 (the first year of widespread ZVL availability and use) or any subsequent years. In this subset (n = 62 395 patients with 130 GCA diagnoses), ZVL vaccination remained a significant risk factor for GCA diagnosis via all diagnostic criteria (HR, 2.35; 95% CI, 1.583.47; P < .0001) and for GCA diagnosis by positive biopsy alone (57 GCA diagnoses; HR, 2.91; 95% CI, 1.575.38; P = .0007).  A copy of the published article is attached as further documentation of the patient's experience.  This is non valid report due to lack of patients' identifiers.