The He lab research focuses on gene regulatory evolution in opportunistic pathogenic yeasts species using the baker’s yeast, Saccharomyces cerevisiae as a model organism. My research aims at answering some of the relevant questions in the field, i. e., what are the genetic factors underpinning the independent evolution of pathogenicity and virulence among budding yeast? Our approach is based on understanding stress response and specifically a phenomenon called acquired stress resistance (ASR), which immunizes organisms to prepare them for the ensuing environmental changes after encountering an initial stressor stimulus. By dissecting the poorly understood genetic basis of ASR, we hope to gain significant insight into how gene regulatory networks evolved and their influence on disease phenotypes among commensal yeasts. Liang at al. from the He lab has shown that, a brief starvation of the pathogenic yeast, Candida glabrata of an essential nutrient; phosphate, induces primary oxidative stress response (OSR) genes. These genes protect it against a severe secondary H2O2 stress. A similar treatment, however, confers little to no benefit in the low pathogenic-potential relative, S. cerevisiae. Interestingly, the transcription factors between ASR and OSR are synonymous, but the combinatorial logic sets are different. Through functional studies, Liang et al. showed that this divergence or differential response to phosphate limitation between Sc and Cg is implicated by the Target-of-Rapamycin Complex 1 (TORC1), through its proximal effector, Sch9 and other unknown upstream regulators. We employe transposing mutagenesis followed by sequencing (Tn-seq) as a genetic screening method coupled with flow cytometry, computational and functional studies to identify these upstream regulators of ASR. Understanding the molecular players in ASR will uncover how the signaling network can be rewired to allow organisms to respond to novel environmental stimuli using existing networks. This will potentially reveal actionable candidate genes implicated in the evolution of pathogenicity and virulence in budding yeast.