The opportunistic human fungal pathogen, Candida albicans is a diploid, dimorphic (yeast-hyphae switch), and commensal organism that colonizes human skin, GI track, and mucosal surface, however, is responsible for severe fungal infections in the immunocompromised. Natural variation occurs among clinical isolates of C. albicans which includes differential virulence associated phenotypic output, gene regulatory network rewiring, and genome sequence heterogeneity. Here we correlated phenotypic differences with gene expression differences to discover a novel transcriptional regulator in biofilm/hyphal regulatory network. Here we identified a new interceding biofilm/hyphal regulator RME1 that had been reported as a positive regulator of chlamydospore formation. Additionally, Tye7 and Gal4, which are known as two main glycolytic activators in C. albicans, lead to rebalancing of regulatory activities among clinical isolates within the species. We found that the balance of activities of Tye7 and Gal4 vary among clinical isolates. Lastly, we investigated a set of 104 bar-coded protein kinase (PK) genes for their biofilm formation ability and the functional basis for their defects by overexpressing either adhesin gene ALS3 or cyclin gene HGC1.