Candida albicans is a diploid fungus. It is largely commensal, but it is also a prominent fungal pathogen within the WHO critical priority group. One of its key virulence attributes is the ability to form biofilms on implanted medical devices, a major cause of disseminated Candida infection. Much is known about the structural and molecular determinants of biofilm formation, as well as their biofilm-associated regulation. Less is known about metabolic features that may support biofilm growth but are not necessary for conventional growth as free-living cells. I focused on a metabolic gene, ERG251, because it is under control of a biofilm master regulator in multiple C. albicans isolates. I find that ERG251 is required for growth in biofilm-like conditions, but not in conventional free-living conditions. The novel aspect of this chapter is the demonstration of what may be the first fungal biofilm-associated metabolic gene. Another key pathogenicity trait is the ability to transition between yeast and hyphal growth. Hyphae are critical for the formation of biofilms and for virulence. Among signals that drive hypha formation is the presence of hemin. I focused on the filamentation response and biofilm formation to hemin addition among C. albicans strains. I found that the response depends upon filamentation regulators Efg1, Brg1, and Rim101, but not upon heme acquisition regulator Hap1 or its target genes. These findings argue that hemin induces hypha formation independently of its utilization. The novel aspect of this chapter is the characterization of a hypha inducing response that may contribute to pathogenicity. A third key virulence factor of C. albicans is the ability to maintain iron homeostasis in the host where iron is scarce. We focused on a master iron regulator, SEF1. We found that iron regulator Sef1 is required for growth, cell wall integrity, and genome integrity during iron limitation. The novel aspect of this chapter is the characterization of strain variation in a circuit that is required for survival in the host, and the connection of iron acquisition to genome integrity.