Finally, PNT1a cells, which are not tumorigenic, can be induced to form tumors in SCID mice by overexpression of either wild type (WT) p65 or p65 S536E in the presence of myristoylated AKT demonstrating synergistic activities of NF-KB and AKT signals in promoting PCa tumorigenesis. The gene discussed is AKT1; the disease is posterior cortical atrophy.