The p53 gene is a widely studied anti-oncogene, or tumor suppressor gene. The p53 gene product can act as a negative regulator of cell growth in response to DNA damage. Mutations and allelic loss of the p53 gene have been associated with malignant transformation in a wide variety of human tumors. p53 shares considerable sequence similarity with p73, a gene that maps to a region in chromosome 1 that is frequently deleted in neuroblastomas. However, p73 does not appear to be activated by DNA damaging agents. The p73 isoform p73α inhibits drug-induced apoptosis in small cell lung carcinoma cells, while the p73 isoform p73β promotes it. p73α also prevents Bax activation, mitochondrial dysfunction, caspase activation and is able to reduce apoptosis induced by the BH3-only protein PUMA (p53 upregulated modulator of apoptosis). There is an equilibrium between p73α and p73β, demonstrated by the fact that p73α inhibits the pro-apoptotic effect of p73β.