Considering that no EVI1 direct binding site was found at the promoter region of GPC1 and that downregulation of miR-96 was reported in pancreatic cancer [25], it might be speculated that EVI1 regulated the expression of GPC1 through miR-96 and that overexpression of KRAS or KRAS mutation also adjusted the expression level of GPC1 in pancreatic carcinogenesis (Figure 2I). The gene discussed is KRAS; the disease is pancreatic neoplasm.