They are largely overexpressed in cancer cells due to transcriptional activation and stabilization through positive feedback loops with upstream regulators, such as the JAK/STAT (Janus kinase/signal transducer and activator of transcription), PI3K/AKT (PI3-kinase/AKT serine/threonine kinase 1), and NF-κB (NF-Kappa-B transcription factor) signaling pathways. This evidence concerns the gene AKT1 and cancer.