This article is available from: http://www.biomedcentral.com/1741-7007/2/5[Background] Excessive proliferation of vascular smooth muscle cells and leukocytes within the artery wall is a major event in the development of atherosclerosis. The growth suppressor p27kip1 associates with several cyclin-dependent kinase/cyclin complexes, thereby abrogating their capacity to induce progression through the cell cycle. Recent studies have implicated p27kip1 in the control of neointimal hyperplasia. For instance, p27kip1 ablation in apolipoprotein-E-null mice enhanced arterial cell proliferation and accelerated atherogenesis induced by dietary cholesterol. Therefore, p27kip1 is a candidate gene to modify the risk of developing atherosclerosis and associated ischaemic events (i.e., myocardial infarction and stroke).[Results] In this study we found three common single-nucleotide polymorphisms in the human p27kip1 gene (+326T>G [V109G], -79C>T, and -838C>A). The frequency of -838A carriers was significantly increased in myocardial infarction patients compared to healthy controls (odds ratio [OR] = 1.73, 95% confidence interval [95%CI] = 1.12–2.70). In addition, luciferase reporter constructs driven by the human p27kip1 gene promoter containing A at position -838 had decreased basal transcriptional activity when transiently transfected in Jurkat cells, compared with constructs bearing C in -838 (P = 0.04).[Conclusions] These data suggest that -838A is associated with reduced p27kip1 promoter activity and increased risk of myocardial infarction.PG was the recipient of a fellowship from the Fundación para el Fomento en Asturias de la Investigación Científica Aplicada y Tecnológica (FICYT, BP 01-082). AD-J received salary support from Fondo Social Europeo (CSICPrograma I3P). This work was supported by grants from the Spanish Fondo de Investigaciones Sanitarias to EC (FIS 03/05) and from the Spanish Ministry of Science and Technology and Fondo Europeo de Desarrollo Regional to VAndrés (SAF2002-1443).Peer reviewed