In light of the growing evidence that AKT3 inhibits cancer cell migration [21] and the fact that AKT isoforms are differentially expressed, with AKT1 being the most abundant AKT isoform in the majority of most breast cancer cell lines [20], inhibitors that preferably target AKT1 and AKT2 might be a promising therapeutic approach. The gene discussed is AKT3; the disease is breast cancer.