Retinoic acid-related orphan receptor (ROR)-gammat, the master transcription factor of the Th17 subset of CD4(+) Th cells, is a promising target for treating a host of autoimmune diseases. RORgammat plays a vital role in the pathogenesis of inflammatory bowel diseases-Crohn disease and ulcerative colitis-caused by untoward reactivity of the immune system to the components of the intestinal microbiome. The mammalian intestinal tract is a highly complex and compartmentalized organ with specialized functions, and is a privileged site for the generation of both peripherally induced regulatory CD4(+) T cells (Tregs) and effector Th17 cells. As Th17 cells can be proinflammatory in nature, the equilibrium between effector Th17 and Treg cells is crucial for balancing intestinal homeostasis and inflammation. Recent findings suggest that RORgammat, in addition to Th17 cells, is also expressed in peripherally induced, colonic regulatory CD4(+) T cells. Therefore, RORgammat is expressed in both effector and regulatory subsets of CD4(+) T cells in the intestine. The present review discusses the role of RORgammat in cellular and molecular differentiation of Th17 and Treg, and examines how targeting RORgammat in inflammatory bowel disease therapy could influence the development of these two diverse subsets of immune cells with opposing functions.