Together, the data show that B56-PP2A activation can counter all mechanisms used by tumor cells to disable 4E-BP1 (i.e., hyperphosphorylation of 4E-BP1, downregulation of 4E-BP1, and increased eIF4E/4E-BP1 ratio) and thereby promote inhibition of eIF4E-dependent translation in multiple cancer cell types. This evidence concerns the gene PTPA and neoplasm.