For example, the up-regulation of some lipogenic genes (e.g., CD36, PPARγ, PGC1α/β, FAS, SCD1, LPL, and VLDLR) may contribute to increased hepatic steatosis and adiposity in deficient GHR-JAK2-STAT5 signaling models, whereas the expression of antilipogenic genes, such as FGF21 and INSIG2, are decreased. The gene discussed is STAT5B; the disease is Hepatic steatosis.