Barth syndrome is a multi-system genetic disorder that affects the mitochondria. It is characterized by a wide range of conditions mostly affecting the heart and skeletal muscles. Symptoms include: cardiomyopathy, skeletal myopathy, neutropenia, increased urinary excretion of 3-methylglutaconic acid and weaker motor skills. What causes the disorder is the mutations in the tafazzin (TAZ) gene, which codes the tafazzin enzyme that, in healthy cells, is widely present in cardiac and skeletal muscles and takes part in the cardiolipin remodeling pathway. Cardiolipin is a phospholipid located in the mitochondrial inner membrane. Unlike other phospholipids, cardiolipin has a specific structure which allows it to interact with a vary of membrane proteins and complexes, giving the molecule important functions in proper mitochondrial energy metabolism. It undergoes a highly conserved and complex synthesis pathway, which is altered in patients with Barth syndrome. Since there exists a lack of understanding the importance and functions of cardiolipin synthesis, Barth syndrome is treated only symptomatically. With improved understanding of the molecular mechanism and importance of cardiolipin synthesis and remodeling, new treatment approaches for Barth syndrome can be evaluated. One such targets may be beta-oxidation. Trimetazadine is a drug widely used for treating heart conditions, which inhibits beta-oxidation and in some previous research influences mitochondrial phospholipid turnover. However, the effect of trimetazidine on cardiolipin synthesis and turnover is unknown. We are curious to see whether the inhibition of betaoxidation promotes mitochondrial phospholipid turnover and increases functional cardiolipin content in cells with TAZ deficiencies. Saccharomyces cerevisiae is a great model organism for studying Barth syndrome because all enzymatic steps in the cardiolipin synthesis and remodeling pathway are conserved form yeast to humans.