Taken together, the differential response to TNF-α between IR and IS individuals in terms of adipogenic capacity can be largely explained by the heightened sensitivity of IR individuals to the insulin resistance-inducing effects of TNF-α, mediated through increased IRS-1 serine phosphorylation and the existing inflammatory state particularly IL-6 and IL-8 within their adipose tissues. The gene discussed is CXCL8; the disease is Insulin resistance.