Studies on antiandrogen-resistant prostate cancer cells showed that IL-1β induces phosphorylation of Tab2 engaged in the nucleus with NCoR complexes, allowing Tab2 to translocate to the cytoplasm together with NCoR, thus dismissing repression from androgen responsive genes and functionally converting antiandrogenic compounds to androgenic [7]. The gene discussed is IL1B; the disease is prostate carcinoma.