By utilizing an autochthonous mouse model of melanoma, Kircher and colleagues showed that hyperactive, ectopic AKT1(E17K) resulted in an enhanced level of brain metastases and reduced overall survival compared to hyperactivating mutations in AKT2 or AKT3, mediated through a FAK an AKT1-specific substrate [32]. The gene discussed is PTK2; the disease is melanoma.