The epithelial-mesenchymal transition (EMT) is a phenotypic change that enables epithelial cells to detach from one another, take on mesenchymal characteristics, and become motile. This process has been implicated in the metastasis of several types of human cancer, including breast cancer. Hypoxia, a condition under which cells are deprived of oxygen, is a common feature of breast tumors due to impaired vascular function and decreased blood flow to the tumor core. Rac1b, a splice variant of the Rac1 GTPase, is over-expressed in breast tumors and has been implicated in the promotion of EMT and the progression of breast cancer. Rac1b signaling activates NADPH oxidase, production of reactive oxygen species (ROS), and expression of EMT transcription factors such as Snail. Rac1b protein must be localized to the cell membrane in order to activate these downstream effectors and promote EMT. This study aims to identify the effects of hypoxia on Rac1b localization and downstream signaling.