In these settings, targeted therapy provoked a robust inhibition of cell proliferation that occurred alongside a highly significant inhibition of PRAS40 and S6 activities, hence suggesting an important role for these molecules, which are downstream effectors of the AKT/mTOR pathway, in the biology of HCC (Figure 3D and Supplementary Table 7). The gene discussed is AKT1S1; the disease is hepatocellular carcinoma.