Therefore, targeting metabolism to prevent breast cancer recurrence has inherent problems: (1) All normal and cancer cells utilize both glycolysis and oxidative respiration for energy requirements; (2) different sub-types of breast cancer have different metabolic requirements and p53 status; (3) the complexities associated with the constant changes in breast metabolism and the emerging cross-talk of p53 with hormone receptors and other signaling pathways. This evidence concerns the gene NR4A1 and breast cancer.