It is now evident that both forms of inflammatory bowel disease (IBD), Crohn’s disease and ulcerative colitis, are highly heterogeneous, not only at the clinical and pathogenetic level, but also in regard to time of appearance. In fact, early- and late-onset IBD are increasingly recognised as distinct entities that can be differentiated in regard to the underlying mechanism of inflammation and response to therapy, both in human patients and in experimental animal models.1^–3 While this differentiation is real, early and late IBD ostensibly result from the combined action of the same factors—that is, genetic predisposition, environmental changes and a disregulated immune response. On this background scenario, Damen and collaborators (Gut 2008;57:1480) ask the very pertinent question of what determines the development of specific effector T cells involved in early gut tissue damage: the expression of specific cell surface receptors or the production of specific cytokines by …