Considering the recent demonstrated role of GLI1 acivation as mediator of the epithelia-to-mesenchymal transition (EMT) and chemoresistance [24–28], and as previous studies demonstrated the effects of metformin on GLI1 activation in breast and pancreatic cancer models [29, 30], we analyzed the GLI1 trascription activity before and after treatment with metformin, MEK-I or both, in our model of NSCLC using a GLI1-responsive promoter within a luciferase reporter expression vector (Figure 2C). Here, GLI1 is linked to familial pancreatic carcinoma.