Whereas the IRF, STAT, and NF-κB pathways were up-regulated by Oxali and potentiated by IFNγ, the MYC and to a lesser extent the AR pathway, both of which participate in PCa tumorigenesis (30, –32), were down-regulated after Oxali + IFNγ treatment. The gene discussed is SOAT1; the disease is posterior cortical atrophy.