NKT cells can rapidly produce a diversity of immunoregulatory cytokines; does this make these cells aggressors or suppressors? New experiments now reveal their immunosuppressive function in tumor control and reiterate their pivotal position. ly suppressing autoimmunity6, and these results have ensured continued debate. Thirteen years after the discovery of NKT cells, we have now moved a step closer to understanding their mechanism of action in at least one type of immune response. In this issue of Nature Immunology, Terabe et al. 1 provide compelling data that defines a new function for CD4+ NKT cells as suppressors of cytotoxic T lymphocyte (CTL)-mediated antitumor immunity. A second, related, study in this issue2 shows that CD4+ T cells that express the NK cell marker, DX5, play a critical role in suppressing delayed type hypersensitivity (DTH). Both of these studies highlight previously unrecognized mechanisms that regulate cell-mediated anti-tumor immunity. Despite our fascination with the spontaneous regression of some human cancers and a plethora of defined tumor-escape mechanisms, investigators have never avidly dissected models in which tumors recur after spontaneous regression. Fortunately, Terabe and colleagues have persisted with their previous observation that a subset of CD4+ T cells could prevent complete CD8+ CTL-mediated eradication of an experimental tumor in mice. By further exploration of this model, Terabe et al. have discovered that these CD4+ T cells are in fact CD1d-restricted NKT cells that specifically prevent effective CTL-mediated tumor eradication in an IL-13–dependent manner1. This study is the first to demonstrate a key role for CD4+ NKT cells, and for IL-13, in the repression of CTL-mediated anti-tumor immunosurveillance. Strikingly, IL-13 mediated its effect via the IL-4R–STAT6 pathway, whereas IL-4–producing capacity was neither sufficient, nor necessary, for NKT cell–mediated tumor repression. A similar pattern of specific dependence on IL-13 in immune clearance of the nematode,