Despite significant advances in therapy for early-stage cancer, the prognosis for most advanced-stage tumors remains little changed over the past 50 years (1). A vast array of novel strategies has been introduced over this period, many of them building on a recent explosion of insights into tumor immunology. Early attempts at cancer immunotherapy focused on IL-2 or other T cell–activating cytokines that were intended to expand the number or potency of T cells specific for tumor-associated antigens (TAAs). Such activated T cells were expected to infiltrate the tumor and lead to the specific destruction of tumor cells. Although these attempts to boost antitumor immunity have yielded some limited examples of tumor regression, they have failed so far to control advanced-stage disease to a significant extent (2). Effective T cell activation depends on the presentation of TAAs by antigen-presenting cells (APCs), such as macrophages, fibroblasts, B cells, or dendritic cells (DCs). Of these, only DCs can prime naive T cells, inducing their differentiation into antigen-specific effector cells. This feature, which was recognized early on, could potentially make DCs ideal agents for promoting TAA-specific immunity. Until recently, however, the rarity of these cells and the inability to cultivate them in large numbers hampered progress in this field. The development of techniques by which DCs can be differentiated ex vivo in large numbers revolutionized their study (3) and led to human trials that demonstrated the beneficial effects of TAA-expressing DCs, at least for some tumors (2, 3). The report of Heiser et al. in this issue of the JCI (4) now provides additional encouraging clinical data that confirm the promise of DC-based immunotherapy.