Notably, inhibiting Rb phosphorylation by antagonizing CDK4/6 was shown to induce AKT activation by releasing Rb-mediated mTORC2 suppression[66] and facilitate metabolic rewiring via mTORC1 to promote glycolysis and oxidative metabolism in pancreatic ductal adenocarcinoma cells[68]. This evidence concerns the gene RB1 and pancreatic ductal adenocarcinoma.