Left: Dectin-1 is expressed on dendritic cells and macrophages, and recognizes molecules called β-glucans (dark green circles) on fungal cell walls. This recognition triggers the signaling pathways that activate transcription factors including IRF5 and NF-κβ (del Fresno et al., 2013), which cause anti-fungal genes to be expressed. Right: Chiba et al. found that Dectin-1 can also recognize N-glycan structures expressed on certain tumor cell lines. Recognizing these tumor cell signals activates IRF5 and perhaps other unidentified pathways, which causes tumoricidal action by natural killer (NK) cells. At least part of the mechanism for natural killer cell mediated tumor killing involves increasing the expression of the Inam gene. It would be interesting in the future to determine if Dectin-1 recognizes N-glycan structures as a proxy for the increased activity of the hexosamine biosynthetic pathway in tumor cells.