Breast cancer will kill approximately 1 in 40 women, making it the second leading cause of death in women. Roughly 50% of HER2 cancers develop drug resistance; this study hopes to fight those statistics. Capsaicin has shown an ability to kill MCF-7 and MDA-MB-231 breast cancer cell lines, but the mechanism of cellular death that it enforces is still unknown. Three different assays were utilized to analyze the possibility of the Warburg Effect playing a role; lipid peroxidase, CyQuant, and oxygen plate analysis. The lipid peroxidase assay showed little change in oxidative stress from the DMSO control and the capsaicin treated cells. The CyQuant assay showed minimal differences in cellular death rates with varying concentrations of capsaicin. The oxygen plate analysis showed that different concentrations of capsaicin had only small changes in oxygen consumption. This data indicates that capsaicin kills cells through an alternate mechanism to the Warburg Effect. Moving forward, data collection will assess the possibility of an alternate pathway in the endoplasmic reticulum: Unfolded Protein Response (UPR), more specifically the activation of IRE1𝛂 protein coupled with GRP78 protein, and the activation of CHOP protein ultimately triggering a caspase cascade that forces cell death.