AKT1 kinase is one of the most frequently activated survival pathways in cancer, and the well‐studied E17K mutation in the pleckstrin homology (PH) domain of AKT1 stimulates downstream signaling and transforms cells, causing AKT1 activation by means of a rapid conformational drift that in turn increases the localization of the protein on the plasma membrane 20, 21. This evidence concerns the gene AKT1 and cancer.