In support of this hypothesis, we have obtained encouraging data at least in cultured pancreatic cancer cells, where one 4E-BP mimic (4E2RCat) efficiently blocked protein synthesis and cell proliferation independently of 4E-BPs levels, while the effects of mTOR inhibitors remained dependent on sufficient 4E-BPs intracellular amounts [4]. Here, MTOR is linked to pancreatic neoplasm.