In response to various forms of intrinsic and extrinsic stresses such as heat shock, electrical stimulation, and viral infection, cells produce non-membrane-bound aggregates of mRNA and proteins called stress granules. These granules sequester mRNA and ribosomal subunits to halt the production of proteins unnecessary for the immediate survival of the cell, thus allowing more energy to be used in combatting the stress. Stress granules are beneficial in the short term, but the chronic presence of stress granules can be cytotoxic. If stress granules are not cleared, hyperaggregation of misfolded proteins, which is thought to play a role in neurological diseases, can occur. After myocardial infarction (heart attack), the heart experiences a lack of oxygen which is known to create free radicals and metabolic stress. Whether the stress response is involved in this process is unknown, as most research on stress granules, especially their role in disease, comes from work in neuronal and cancer cells. To test whether the stress granules response is conserved across cell types and how cardiomyocytes (heart muscle cells) specifically respond to stress, I cultured cancer cells, embryonic stem cells, and embryonic stem cell-derived cardiomyocytes and subjected these cells to various forms of stress, including sodium arsenate poisoning and heat shock. Using fixed immunofluorescence and spinning disk microscopy, I imaged each treatment and quantified the number of stress granules per cell. The sodium arsenate treatment induced stress granule formation in all three cell types, but surprisingly, the heat shock treatment only induced stress granule formation in the stem cells. It is widely believed the stress response is conserved across a wide range of cell types, but these results indicate some stress pathways differ between cardiomyocytes, cancer cells, and stem cells. Future experiments will test additional types of stress and how stress granules contribute to cardiomyocyte function.