This synergism in the action of anti-cancer drugs and PUFAs on cancer cells could be attributed to their ability to enhance lipid peroxidation process and alter the status of anti-oxidants (Tables 1 and 2), though it has also been attributed to changes in the formation/concentrations of eicosanoids, PPARs, protein kinase C/extracellular signal regulated kinase pathway-dependent induction of c-Myc expression, Bbl-2 expression and Gs-axin-beta-catenin signaling axis in tumor cells [24], [25], [27]–[41]. This evidence concerns the gene MYC and cancer.