IL-6 Variants in Ischemic Stroke

published from 2007 onward [7] . On the other hand, the results cited in the article appear to have been muddled. Thus, a study by Flex et al. [8] refers to an entirely different phenotype of peripheral artery occlusive disease (only 22 patients actually also had a history of stroke). Assuming that the authors had intended to refer to another study by the same author [9] , we face the obvious overlap of cases and controls with a further investigation [10] . Similarly, overlap of cases and controls was ignored for the studies by Revilla et al. [11] and Chamorro et al. [12] . The number of cases and controls pooled is thus inflated. Another issue that has been overlooked is the sharp discrepancy in –174C allele frequencies in the studies by Yamada et al. [13] and Tong et al. Dear Editor, I have read with interest a recent report by Kumar et al. [1] on the putative role of interleukin-6 (IL-6) in ischemic stroke. In their report, the authors refute an association of 2 promoter variants on the phenotype under study based on earlier case– control investigations. Data from this article, however, warrant a reappraisal of existing findings. On one hand, numerous investigations were not retrieved. A quick search using the same databases as employed by the authors unveiled additional studies both for –572G/ C [2, 3] and for –174G/C [4–6] and around 10,000 additional genotypes that had been available at the time of the August 30, 2014, data freeze. I am not even counting the genome-wide association studies that were Received: August 8, 2015 Accepted: December 22, 2015 Published online: March 11, 2016