Research in Crohn disease (CD) and ulcerative colitis (UC), together known as the inflammatory bowel diseases (IBD), has truly seen a revolution in the last 5-10 years. This book examines how these genetic discoveries have led to the identification of biological functions not previously associated with IBD pathophysiology (e.g. autophagy), how multiple genetic risk factors for IBD converge on given biological functions and that together the identified variants in these genes have predisposing and protective roles (e.g. the multiple variants in the receptor for the IL23 cytokine and its signaling cascade), and how having such a large number of known genetic risk factors has changed our understanding not only about the genetic and molecular overlap between CD and UC, but also between these diseases and other chronic inflammatory diseases (e.g. psoriasis,  multiple sclerosis, type 1 diabetes and many others).