We provide evidence that the FAK-mediated decrease of AKT activity by 4HPR treatment, as well as AKT inactivation/activation with Wortmannin or LY294002 and IGF-I or Myr.Akt, respectively, tightly controls the chemotactic and metastatic phenotype of androgen-independent prostate carcinoma cells and may also explain the already described suppression of constitutive NF-kB activation, mediating invasion and osteoclastogenesis, in human prostate cancer cells exposed to 4HPR [12,37]. The gene discussed is PTK2; the disease is prostate carcinoma.