Toll-like receptors (TLRs) are an important link between innate immunity and a variety of clinical disorders, includ-ing cardiovascular diseases. 1,2 Experimental studies have shown that TLRs might be involved in the development of left ventricular (LV) remodeling induced by pressure overload. For instance, TLR4 knockout mice developed less-severe LV remodeling following aortic banding than matched wild-type animals, 3 whereas blockade of MyD88, an intermediate factor of TLR pathway, also attenuated load-induced cardiac growth. 4 In addition, recent evidence revealed that TLRs mediate LV remodeling and dysfunction in ischemic hearts, 5,6 strengthen-ing the concept that these receptors might be key regulators of cardiac structure following myocardial injury. There are currently 11 known human TLRs, each of them contributing to specific recognition of particular pathogen-associated molecular patterns. 1 TLR6 forms heterodimers with TLR2 for recognition of microbial components and acti-vates intracellular signaling pathways related to inflammatory response and cell growth. 7 Previous studies identified a coding polymorphism in the TLR6 gene that leads to an exchange from serine to proline at position 249 in the extracellular domain of the protein. 8 This variant was associated with a reduced risk of asthma 8,9 and an increased risk of invasive aspergillosis, 10 but was not related to myocardial infarction. 8 Nevertheless, no The first two authors contributed equally to this work. Background Experimental data demonstrated that inactivation of toll-like receptor (TLR) pathway components attenuated left ventricular (LV) remodeling induced by pressure overload. This study investigated the impact of TLR6 Ser249Pro polymorphism on LV structure in hypertensive subjects.