Given that c-MYC (here-after called MYC) is highly expressed in prostate cancer (20, 21), is a potent driver of growth and proliferation (22), and yet has been described as ‘undruggable’ (23), we have been particularly interested in determining whether BAT can reduce MYC expression and understanding the relative contribution of downregulation of MYC toward growth inhibition by SPA. The gene discussed is MYC; the disease is prostate carcinoma.