In their study, metformin-treated cancer cells were less sensitive to growth following IGF-1 stimulation and displayed increased activity in PP2A phosphatase which deactivates p70S6K, a kinase downstream of mTOR signaling.[22] In pancreatic cancer cell lines, potential crosstalk exists between the insulin/IGF-1 stimulated PI3K/AKT/mTOR pathway and the GqPCR stimulated mTOR pathway. The gene discussed is MTOR; the disease is pancreatic neoplasm.