Interestingly, theaflavins offered better protection to T helper cells from tumor-induced death in comparison to either celecoxib or Cox-2-siRNA suggesting that along with PGE2, tumor-induced CD4+ T cell death might have other mediators that are independent of Cox-2 and inhibition of not only PGE2 but also those mediators by theaflavins could be the cause behind observed immunoprotection provided by these polyphenols. The gene discussed is CD4; the disease is neoplasm.