In mutant-RAS cancer cells, high ROS levels can result from increased metabolic activity of peroxisomes, oxidases, cyclooxygenases (COX), lipoxygenases (LOX), from mitochondrial dysfunction, or they can derive from the cross-talk with infiltrating immune cells and other components of the tumor microenvironment (TME) (Szatrowski and Nathan, 1991; Babior, 1999; Storz, 2005). This evidence concerns the gene LOX and cancer.