IL1B and infection: 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.