During fungal infection, a variety of receptors initiates immune responses, including TLR and the beta-glucan receptor Dectin-1. TLR recognition of fungal ligands and subsequent signaling through the MyD88 pathway were thought to be the most important interactions required for the control of fungal infection. However, recent papers have challenged this view, highlighting the role of Dectin-1 in induction of cytokine responses and the respiratory burst. Two papers, using independently derived, Dectin-1-deficient mice, address the role of Dectin-1 in control of fungal infection. Saijo et al. [1] argue that Dectin-1 plays a minor role in control of Pneumocystis carinii by direct killing and that TLR-mediated cytokine production controls P. carinii and Candida albicans. By contrast, Taylor et al. [2] argue that Dectin-1-mediated cytokine and chemokine production, leading to efficient recruitment of inflammatory cells, is required for control of fungal infection. In this review, we argue that collaborative responses induced during infection may partially explain these apparently contradictory results. We propose that Dectin-1 is the first of many pattern recognition receptors that can mediate their own signaling, as well as synergize with TLR to initiate specific responses to infectious agents.