The discovery of p73 as a family member of p53 has instigated a number of studies in search of its function, regulation, and involvement in tumorigenesis. p73 has been identified as a transcription factor that can regulate p53-dependent transcriptional targets. Similarly to p53, p73 can induce apoptosis in response to various stimuli, including certain types of DNA damage. This evidence suggests that p73 may act as a tumor suppressor with overlapping functions of p53. While mutations of p73 appear rare in human tumors, some leukemias have shown silencing of the gene by hypermethylation. Thus, introduction of p73 into tumor cells possessing inactive p53 may provide a valuable therapeutic approach.