Dectin-1 signaling triggers the segmentation of pro-IL-1β, resulting in the ultimate production of IL-1β through activation of NLRP3 and caspase-1 or caspase-8 inflammasome pathways.12–14 The NLRP3 inflammasome is potentiated by diverse activators and recognizing patterns, including damage-associated molecular patterns (DAMP), and pathogen-associated molecular patterns (PAMP), which are targets of fungi, bacteria, and viruses.15 Subsequently, downstream immune response is triggered by these activators in the different circumstances, including fungal invasions and infections. This evidence concerns the gene NLRP3 and infection.