The overall goals of the current investigation were (1) to determine a potential mechanism by which blocking the activity of STAT3 and STAT5 affects system xc-, given the dynamic involvement of these particular transcription factors with mitochondrial function, redox balance, and the regulation of other key factors associated with cellular metabolism, which are all processes potentially interconnected with xCT expression, and (2) how these changes ultimately affect the genetic profile of different cancer cell types. The gene discussed is STAT3; the disease is cancer.