Given that iron dysmetabolism has been demonstrated to play an important role in driving the pathogenesis of prostate cancers [23], as well as recent findings implicating FTH1 as having nontrivial tumor suppressive properties [24], we sought to expose LNCaP AR-positive and PC3 AR-negative prostate cancer cells to SPH and/or bicalutamide to investigate whether, and to what extent, this strategy would inhibit cancer cell proliferation via gene regulation. The gene discussed is AR; the disease is neoplasm.