Consistent with a direct transcriptional regulation of p110α PI3 kinase expression, TBL1 knockdown was able to also impair p110α PI3 kinase protein levels under these conditions as well as the activity of prototypical PI3 kinase targets, including protein kinase B/Akt and glycogen synthase kinase (GSK) 3, in pancreatic cancer cells, while levels of the PI3 kinase antagonist PTEN remained unchanged (Fig5; Supplementary Fig S12). This evidence concerns the gene AKT1 and pancreatic neoplasm.