Possible explanations for these discrepancies between our data and clinical data include (1) subtle differences in expression of secretory kinetics that were not evident from our screen; (2) that these differences were masked by screening in a non-physiological cell type; (3) that coding variants of leptin artificially lower serum leptin detection through changes in ELISA antibody affinity; and (4) that the coding variants do not influence serum leptin and other genetic causes explain obesity in these cases. This evidence concerns the gene LEP and obesity disorder.