Dyslexia is a type of learning disability which effects word reading accuracy, fluency and comprehension. Dyslexia affects approximately 10% of Australians and is the most common cause of reading, writing and spelling difficulties. Additionally, it is a highly heritable disorder with estimates from twin studies indicating a heritability of approximately 70%. A genome wide association study (GWAS) which estimates the association between common variants and disease has recently been published for dyslexia utilising 51,800 self-reported cases and 1,087,070 controls. Current treatment for dyslexia involves learning support tools and teaching techniques, while no pharmaceutical targets are available. Identifying genes associated with changes in disorder risk could reveal biological mechanism related to dyslexia. GWAS can be utilised in combination with expression quantitative trait loci to model the effects of genetically regulated expression on dyslexia through a transcriptome-wide association study (TWAS). Across 14 tissue types (N=100-558) from the brain and whole blood we identified 112 unique signals which were associated with dyslexia after multiple testing correction. Conditional analysis which is used to adjust for the predicted expression of nearby genes further refined this to 56 conditionally independent genes. Although these genes are associated with dyslexia, further evidence is required to determine if they may causally influence disorder pathology. Bayesian fine-mapping is an approach which identifies credible sets of genes with a 90% probability of containing the true causal gene if such as gene exists within the region investigated. We identified 21 genes with strong evidence (PIP > 0.8) of potentially causally influencing dyslexia. Triangulated these results highlights 3 genes (COMMD7, COG5, GNAQ) which were both TWAS conditionally independently associated and possessed strong evidence from fine-mapping. Exploring the role of these genes and how they may functionally relate to dyslexia could reveal novel insights into disorder pathophysiology.