It increases the levels of pro-inflammatory molecules like interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α), which drive endothelial dysfunction, neuroinflammation, cardiac fibrosis, and heart failure [9,15,16,17,18,19,56] and can affect important regulatory areas like the insular cortex, thus exacerbating cardiac dysregulation [16]. The gene discussed is TNF; the disease is endothelial dysfunction.