The crosstalk between inflammation and metabolic dysfunction, such as the interaction between TNF-TNFR1 and LPS-TLR4 pathways with insulin signaling impairment (23, 28), mitochondrial dysregulations (36, 37), and autolysosomal defects (22, 38, 39), may provide more insights to the pathogenesis of obesity-induced neuroinflammation and neurodegeneration through body-brain interaction. The gene discussed is TNF; the disease is obesity disorder.