Fungi pose a serious threat to human health, with Candida albicans as both a leading fungal pathogen of humans and a member of the human mucosal microbiome. A major virulence trait of C. albicans is its ability to transition between yeast and filamentous morphologies. The yeast form of C. albicans is crucial for colonization and dissemination via the bloodstream, while the filamentous form enables tissue invasion and deep-seated infection. Here, I discuss recent work exploring genomic analyses that implicate core regulators of proteostasis in governing temperature-dependent morphogenesis. I also discuss recent work that identifies determinants of C. albicans filamentation in host immune cells, given that internalization of C. albicans by macrophages induces a transition from yeast to filamentous growth that promotes macrophage cell death and fungal escape. The filamentation response within macrophages has been attributed to conditions within the phagosome such as nutrient deprivation, alkaline pH, and oxidative stress, however, the impact of other host-derived factors has remained unknown. Here, I show that lysates prepared from macrophage-like cell lines robustly induce C. albicans filamentation and implicate a phosphorylated, immunomodulatory peptide. I discuss the relationship between filamentation and cell wall remodelling in the induction of pyroptosis, a macrophage inflammatory cell death program. Together, this work explores mechanisms governing a key virulence trait that is central to a complex host-pathogen interaction.