According to these results, our group demonstrated that, in twenty-nine cancer cell lines with different histological origin (melanoma, n = 7; Breast Cancer (BC), n = 6; Non-Small Cell Lung Cancer (NSCLC), n = 6; ColoRectal Cancer (CRC), n = 8; pancreatic adenocarcinoma, n = 2), PTEN-loss predicts synergistic interaction between MAPK (trametinib, dabrafenib) and PI3K/mTOR (everolimus, MK-2206, gedatolisib) pathway inhibitors, while combined MEK/mTOR inhibition results in a slightly additive/frankly antagonistic growth inhibitory response in PTEN-competent tumor cells (Table 2) [78]. This evidence concerns the gene PTEN and pancreatic adenocarcinoma.