In T2D, chronic hyperglycemia, salt-sensitive hypertension and obesity produce metabolic, hemodynamic and lipotoxic effects described as main activators of intracellular signaling pathways such as nuclear factor kappa–B (NF-κB), Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) and nuclear factor erythroid 2-related factor 2/heme-oxigenase-1(Nrf2/Hmox-1) [9,10,11,12]. This evidence concerns the gene NFE2L2 and type 2 diabetes mellitus.