Sub-lethal concentrations of VK3 and AA, together with αTOS at a sub-apoptotic dosage, have previously been shown to efficiently induce prostate carcinoma cell death as a result of DNA fragmentation, lysosomal/mitochondrial perturbation, and cytochrome c release, but in the absence of appreciable caspase activation [5, 13]. This evidence concerns the gene CYCS and prostate carcinoma.