If glitazones (PPARγ agonists) are important to induce antiproliferative or proapoptotic effects in cancer cells taking advantage of the inhibition of glycogen synthase kinase-3β (GSK-3β), a crucial activator of nuclear factor-kappaB (NF-kB), at the same time PPARγ agonists provoke several physiological modifications that influence lipid metabolism, glucose homeostasis and activation of inflammation signaling cascade (Figure 3). This evidence concerns the gene PPARG and cancer.