Further evidence of the involvement of CDK4/6 inhibitors in glucose metabolism comes from studies of pancreatic ductal adenocarcinoma, where pharmacological CDK4/6 blockade leads to a marked increase in both glycolytic activity and oxidative phosphorylation together with mitochondrial expansion and the increased production of ATP and reactive oxygen species [17]. This evidence concerns the gene CDK4 and pancreatic ductal adenocarcinoma.