PLAU and lung adenocarcinoma: Interestingly, p38/MAPK inhibition could block the KLF17-induced reduction of p-p38/MAPK and uPA in the KLF17-overexpression group, which suggests that p-p38/MAPK and uPA are downstream target molecules of KLF17 and that the p38/MAPK pathway is required for KLF17 to suppress uPA in lung adenocarcinoma.