Beyond the well-known function of poly(A) tail length in mRNA stability, recent years have witnessed an explosion of information about how changes in tail length and the selection of alternative polyadenylation sites contribute to the translational regulation of a large portion of the genome. The mechanisms and factors mediating nuclear and cytoplasmic changes in poly(A) tail length have been studied in great detail, the targets of these mechanisms have been identified--in some cases by genome-wide screenings--and changes in poly(A) tail length are now implicated in a number of physiological and pathological processes. However, in very few cases have all three levels--mechanisms, targets and functions--been studied together.