Functionally, this interaction translates to an increase in p53-induced cell cycle arrest or apoptosis, as demonstrated by fibroblast growth arrest following TAF9 overexpression, UV-induced association of p53 with TAF9 (45), and TAF9-induced apoptosis of neuroendocrine tumor cells deprived of nerve growth factor (124). This evidence concerns the gene TAF9 and neuroendocrine neoplasm.