In cancer, AKT is aberrantly activated throughPI3K-AKT pathwaystimulation by upstream receptor tyrosine kinases and/or PI3K/Rasmutations, and AKT gene amplification.−, ,  AKT mutations are less common but enhancethe oncogenesis of breast, uterine, colorectal, and prostate cancers., As such, AKT stands as an attractive drug target. This evidence concerns the gene AKT1 and cancer.