They say you can pick your friends, but not your family. The same may hold true for related proteins. The protein TAp73 is a relative of the well-known, tumor-suppressor protein p53. It shares extensive common gene sequences with p53 and, as suggested by some previous studies, it may function similar to p53 to prevent tumor formation. However, unlike p53, which is the most commonly mutated gene in human tumors, TAp73 is rarely mutated, and instead is frequently overexpressed in a wide range of human tumors, including breast, colon, lung, stomach, ovarian, bladder, liver, neuroblastoma, glioma, and leukemias. In other words, cancer cells may have too many copies of the TAp73 gene. Researchers still do not know whether TAp73 enhances tumor cell growth and, if so, exactly how it may give an advantage to tumor cells. But, in a new study that appears in Nature Cell Biology, Xiaolu Yang, PhD, professor of Cancer Biology at the Perelman School of Medicine, University of Pennsylvania, and the Abramson Family Cancer Research Institute, and colleagues found that TAp73 supports the proliferation of human and mouse tumor cells. They also identify an important mechanism by which TAp73 gives tumor cells a growth advantage: it activates the expression of an enzyme called glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting molecule of the pentose phosphate pathway (PPP).