AKT1 and neoplasm: This network is then co-opted by tumours in malignancy, where mutations in the receptor tyrosine kinases upstream of phosphoinositide 3-kinase (PI3K) (e.g., EGFR and HER2), the p110α catalytic subunit of PI3K, the downstream kinase Akt, and the negative PI3K regulator phosphatase and tensin homologue (PTEN) are frequently observed in cancers [32].