In preadipocytes with high levels of beta-catenin, TCF7L2 overexpression is associated with greater beta-catenin binding that facilitates WNT activation and inhibition of adipogenesis whereas in mature adipocytes, with low levels of beta-catenin, it is TCF7L2 gene downregulation that activates WNT pathway leading to similar metabolic effects such as adipocyte hypertrophy, increased fat deposition in the liver and insulin resistance (11). The gene discussed is TCF7L2; the disease is Insulin resistance.