TNF-α is responsible for the progression of T1DM and T2DM through the prevention of glucose-induced insulin secretion and the destruction of β-cell function and inducing apoptosis.23 It was pointed that abnormal conditions like hyperglycemia and enhanced oxidative stress can stimulate the activation of the protein complex of the JNK (c-Jun N-terminal kinase) pathway and the NF-κB (nuclear factor Kapa B) signaling, which can release the pro-inflammatory mediators such as IL-6 and TNF-α.24,25. This evidence concerns the gene NFKB1 and Hyperglycemia.