Candida albicans is a common commensal fungus that colonises the body's mucosal surfaces. In healthy individuals, C. albicans rarely causes disease and infections are usually limited to superficial or relatively easy-to-treat infections. However, in immunocompromised individuals, C. albicans can cause severe and life-threatening infections such as candidemia or systemic candidiasis, where mortality can reach upwards of 60%. Our bodies deploy several immune strategies to combat C. albicans infection; however, recent studies suggest a non-redundant role of the NLRP3 inflammasome in antifungal defence. During infection, activation of the NLRP3 inflammasome leads to activation of caspase-1, which coordinates potent inflammatory responses by pro-IL-1β/IL-18 into their mature, bioactive forms and also cleaves gasdermin-D to induce an inflammatory form of cell death termed pyroptosis. C. albicans targets pyroptosis to mediate its escape from within infected cells; however, by doing so, it also drives a potent inflammatory response, which ultimately favours the host and leads to fungal clearance. While the NLRP3 inflammasome plays an essential role in mediating the anti-fungal response, aberrant signalling also drives several debilitating inflammatory diseases. Thus, several NLRP3 inflammasome inhibitors are already in preclinical development. Given that NLRP3 inhibitors will soon enter the clinic, it is essential that we understand how they may alter host immunity in the context of C. albicans infection. Using bone-marrow-derived macrophages treated with MCC950, an NLRP3 inhibitor, or VX-765, a caspase-1 inhibitor, we found that the inflammatory response to intracellular infection with novel C. albicans clinical isolates was ablated; however, infected cells were not protected from cell death. Interestingly, we found that mice treated with MCC950 and then infected with C. albicans suffered from a higher fungal burden in the kidneys. These findings offer valuable insight into balancing the therapeutic benefit of inflammasome inhibition to treat underlying disease with the heightened susceptibility to C. albicans infection.