Current research suggests that the neurobiological substrate of dyslexia involves the dysfunctional orchestration of a multi-dimensional and hierarchical circuitry of at least three neuronal networks. This circuitry principally involves the posterior corpus callosum, left arcuate fasciculous, and the right frontostriatal attentional control network. The key to understanding the disability and in forging a comprehensive theory of dyslexia may be found in investigations aimed at interactions among all three networking territories.Keywords: Dyslexia; Corpus callosum; Arcuate fasciculus; Frontostriatal attention control Developmental dyslexia is a hereditary, neurocognitive-based learning difficulty, usually identified early in children's primary education when young children struggle to acquire proficiency in beginning reading skills. Prevalence estimates vary, ranging from 5% to as high as 20% [1]. After more than a century of research and the implementation of a broad range of remedial strategies, this disability, which affects individuals irrespective of their level of intelligence, motivation to learn and adequate educational and social circumstances, remains relatively intransigent to educational approaches. The reading, spelling, and array of related cognitive difficulties found in children with dyslexia persist into adulthood [2]. Familial studies indicate an etiological origin in an intricate interplay of neurobiological, genetic, epigenetic, and environmental factors [3].