Although I believe that the role of Ebf1 in adipocyte inflammation is a completely separate process than its role in differentiation, the two processes become intertwined when attempting to deconvolute human EBF1 studies: innately low EBF1 expression or activity will likely impair adipogenesis, which will almost certainly lead to metabolic disease; but higher or just “normal” levels may permissively foment WAT inflammation, also leading to insulin resistance and metabolic disease. The gene discussed is EBF1; the disease is Insulin resistance.