Underlying the phenotypic alterations in HF offspring are gene expression changes, such as the upregulation of phosphoenolpyruvate carboxykinase (PEPCK) that mediates gluconeogenesis [12] and stearoyl-Coenzyme A desaturase 1 (SCD1) [13] that mediates lipogenesis in the liver, and downregulation of the peroxisome proliferator-activated receptor gamma (PPAR-γ) [7], a critical regulator of peripheral insulin resistance that promotes triglyceride storage and reduces free fatty acid (FFA) release in the white adipose tissue. The gene discussed is PPARG; the disease is hydrops fetalis.