In our study, we found that overexpression of Sema3E induced greater phosphorylation of ERK1/2 in MiaPaCa-2 cells, and that treatment of MiaPaCa-2 cells with trametinib suppressed cell proliferation to a greater extent in Sema3E-overexpressing cells, thereby suggesting that the MAPK/ERK pathway could be one of the mechanisms involved in the proliferation of Sema3E-overexpressing pancreatic cancer cells. The gene discussed is SEMA3E; the disease is pancreatic neoplasm.