Ocular surface disease is a widespread and increasingly appreciated disease entity, which may reduce quality of life for patients. Epithelial disease and reduced corneal epithelial barrier function can be caused by inflammation [1], mediated by various cytokines and chemokines in the tear fluid including interleukin (IL)-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, interferon (IFN)-γ and tumor necrosis factor (TNF) [2]. Studying inflammatory cytokines and the proteome of biological fluids to screen for disease-specific biomarkers has been in focus over the past decades [3,4] through flow cytometry and liquid chromatography mass spectrometry (LC-MS) [5,6]. We have previously analyzed the tear fluid biochemically in patients with congenital aniridia [7] and patients with primary Sjögren's syndrome compared to healthy controls [8,9], as well as compared tear fluid proteomics in Sjögren's syndrome and non-Sjögrens syndrome sicca patients [3], which resulted in the detection of potential novel disease biomarkers [3]. However, knowledge is lacking about the normal variation and heritability of tear fluid inflammatory markers. Further inquiries into this field may help identify disease- or genome-specific biomarkers for use in diagnostics and monitoring of ocular surface disease treatment. As genome-wide association studies require large resources and sample sizes and are less generalizable to other ethnic groups than the ones studied, classical heritability studies may aid by pointing to specific areas of interest for future research [10]. For this reason, we conducted a study on the heritability of tear fluid inflammatory cytokines in healthy individuals.