The complex interaction between oxidative stress and AGEs affects many signaling molecules and systems such as TGF-β, NF-κB, activator protein-1 (AP-1), the transcription factor specificity protein-1 (SP-1), and the renin–angiotensin system through AGE/RAGE signaling, which provokes chronic inflammation, glomerular and tubular hypertrophy, and consequently augments renal failure (Lee and Park, 2013; Tiwari et al., 2013). The gene discussed is JUN; the disease is acute kidney injury.