Moreover, pre-clinical studies, in different tumors suggest that co-targeting of MAPK and PI3K/mTOR pathways may be a potentially promising strategy, as shown by results obtained in gefitinib-resistant NSCLC cells [34], in pancreatic cancer cells [35], in rhabdomyosarcoma cells [36], in NRAS mutant melanoma cells [17] and in BRAF mutant melanoma cells with acquired resistance mediated by upregulation of PDGFRβ [16]. This evidence concerns the gene MTOR and familial pancreatic carcinoma.