These pathological processes are intricately linked to the diabetic microenvironment, where hyperglycemia induces reactive oxygen species (ROS) accumulation, promotes the activation of nuclear factor-κB (NF-κB), and upregulates pro-inflammatory cytokines such as TNF-α and IL-6, thereby perpetuating a vicious cycle of inflammation and tissue degradation. This evidence concerns the gene TNF and Hyperglycemia.