Dyslexia is a very common developmental disorder. The aetiology of this complex disorder must in large part still be clarified. Dyslexia segregates in families and the risk for a sibling to become dyslexic is 3.5-fold increased. Different phenotypic dimensions are correlated with dyslexia. These are mainly phonological awareness, phonological decoding, orthographic coding, auditory short-term memory, and rapid naming. The correlated dimensions segregate in families and were found to be heritable. The heritability of word reading lies between 50% and 60%, and that of spelling between 50% and 70%. Based on genome wide linkage analyses, nine candidate gene regions (DYX1-DYX9) could be identified. Recently, four candidate genes, DCDC2, KIAA0319, ROBO1 and DYX1C1 were identified by systematic association analyses. All these genes play a function role in neuronal migration, making them promising candidate genes for dyslexia. However, a functionally relevant mutation has not yet been identified. The comorbidity between dyslexia and ADHD and between dyslexia and SLI could be explained, at least in part, by genetic factors. For future research, all relevant factors playing a functional role in dyslexia should be investigated in sufficiently large samples. This research should integrate genetic, neurobiological, and environmental factors. For an understanding of causes, it is very helpful to understand the interaction between different factors, namely gene-environmental and gene-gene interaction. In a recent project funded by the EU in the Sixth Framework (www.neurodys.com), the worldwide largest sample of children with dyslexia will be sampled and investigated. The goal of this project is to investigate the biological basis of dyslexia in order to improve the basis for the development of successful diagnostics and therapies.