Candida albicans is defined as one of four “critical priority” fungal pathogens that cause life-threatening infections in immunocompromised patients. In these patients, the formation of surface-attached C. albicans biofilms on medically implanted devices is associated with antifungal drug resistance, candidemia (fungal sepsis), and an increased mortality rate. In this project we show, for the first time, that C. albicans can form liquid-suspension (CaLS) biofilms that are morphologically and transcriptionally distinct from surface-attached biofilms. We show that CaLS biofilms form in mammalian cell culture media at 37 °C when no surface is available for adherence, either from planktonic cells or from mature surface-adhered biofilms. Confocal imaging of formalin-fixed paraffin-embedded CaLS sections revealed dense cell clusters with heterogeneous morphologies (hyphal and yeast cells), connected to one another through extensive hyphal networks. To determine how CaLS biofilm is regulated at the transcriptional level, we performed RNA-seq on CaLS and surface-adhered biofilms at establishment and mature time points. We also screened a library of 158 homozygous non-essential transcription factor mutants for their ability to form CaLS biofilms using dissection microscopy, viability assays, and machine learning-powered imaging analysis. These experiments showed that iron regulation, cell aggregation, and cell dispersal genes play a unique role in CaLS biofilm formation, in addition to previously characterized C. albicans master biofilm morphology regulators. Additionally, surface-adhered biofilms became transcriptionally more similar to CaLS biofilms over time, highlighting a possible role for CaLS in biofilm dispersal.