Anti-PCa activity of DI in vivo was examined in male TRAMP mice. In vitro DI stimulated phagocytosis and expression of a panel of inflammatory mediators (C4b, CXCL3, lymphotoxin, NOS2, TLR1, TNF, and TNFSF14) in cultured macrophages and increased tumor killing of both macrophages and TRAMP mouse splenocytes. The gene discussed is TNF; the disease is posterior cortical atrophy.