Genome-wide association (GWA) studies are substantially improving our understanding of the molecular pathways leading to inflammatory bowel diseases (IBD). This is a result of the nature of these studies, which are comprehensive – leading to a dramatic increase in the number of validated genetic risk factors – and unbiased – leading to the identification of novel pathways not previously suspected in IBD. Such discoveries are not only driving the functional studies to understand the mechanisms by which genetic variants modify an individual's susceptibility to disease, but also hold the promise of guiding the development of more effective treatment strategies. In this review, we discuss how GWA studies are enabling us to rewrite the story of IBD pathogenesis, focusing on the interleukin-23 and autophagy pathways.