Under obese conditions, TNF-α promotes insulin resistance via following mechanisms: (i) phosphorylation of IRS-1, (ii) enhanced hepatic glucose synthesis by augmenting adipocyte lipolysis and free fatty acid synthesis, (iii) downregulation of adiponectin levels, (iv) upregulation of IL-6 levels and (v) inhibition of preadipocyte differentiation to adipocytes by suppressing PPAR-γ levels, which in turn promote infiltration of uncommitted cells and expansion of adipose tissue mass [31]. The gene discussed is IRS1; the disease is Insulin resistance.