We extended the work by the McGraw lab10,25 and demonstrated that in primary mouse adipocytes differentiated in vitro, in primary human adipocytes differentiated in vitro, and in mouse Neuro-2a neuroblastoma cells that chronic GIPR agonism impairs the ability of cells to produce cAMP in response to subsequent stimulation and this functionally results in the impairment of GIPR function to increase FA uptake into adipocytes. The gene discussed is GIPR; the disease is neuroblastoma.