Inflammatory bowel disease (IBD) is a multifactorial disease characterized by abnormal immunologic responses to intestinal antigen, and its causes have not yet been clarified. IBD is known to be due to a complexity of environmental, genetic, and abnormal immunological responses. The hygiene hypothesis remains the key hypothesis for explaining the increase in the incidence of IBD, and smoking is the strongest of the known external environmental factors. Since the detection of the NOD2/CARD15 gene in 2001, rapid progress has occurred, and recently, an important relation between the IL23R gene and IBD has been established. Although studies of normal flora in IBD have some difficulties in methodology, the theory that the loss of immune tolerance to normal flora in the bowel results in IBD is still believed. Incomplete adaptation of innate and adaptive immunity is also one of the important pathogenesis. The toll-like receptor family and the NOD-like receptor family have a important role in the pathologic condition. As to adaptive immunity, in Crohn's disease, the Th1 phenotype is known to be involved, and in ulcerative colitis, the Th2 phenotype cytokines are known to be involved. However, recently, the roles of new cytokines and variable phenotypic lymphocytes have attracted interest. We can clarify the relations of inflammatory pathway-specific and molecular classification of the phenotypes of patients in 10~20 years if progress continues at the same rate as during the last 10 years. We also expected to develop a new therapeutic approach based on these efforts.