Volatile anesthetics are widely used in medical practice, however their specific mechanism of action remains unknown. A number of model systems have been utilized to elucidate the target molecules and pathways affected by volatile anesthetics, including Saccharomyces cerevisiae, the bakers yeast. Volatile anesthetics have been demonstrated to inhibit cell growth of S. cerevisiae when present at a specific minimum atmospheric concentration. Furthermore, yeast carrying mutations in various genes involved in ubiquitin metabolism are resistant to normal inhibitory concentrations of anesthetic. Amino acid permeases present in the plasma membrane are also involved in volatile anesthetic resistance. Amplification of the Tat1 permease gene has been shown to increase anesthetic resistance. It is known that ubiquitination of plasma membrane proteins targets them for proteasomal degradation, offering a possible link between ubiquitin metabolism and amino acid uptake. Previous studies have shown that phenylbutyrate has a growth inhibiting effect on yeast through inhibition of amino acid uptake. In this study, it is proposed that phenylbutyrate shares a common mode of action with the anesthetic isoflurane, such that when a critical amount of phenylbutyrate is present, the normal anesthetic response will be observed in isoflurane resistant yeast cells. To test this, yeast cells were spotted on synthetic complete media supplemented with phenylbutyrate, and then grown in an isoflurane atmosphere. The study found that a 12% isoflurane atmosphere was a critical concentration in distinguishing wild-type cells from resistant. In addition, when present at 0.08 - 0.10 mM concentrations, phenylbutyrate was able to increase sensitivity to isflurane. Further study is required however, to confirm these results.