In rodent models of chronic kidney disease there is increased Socs2 gene expression in liver and muscle, which may contribute to impaired phosphorylation and nuclear translocation of GH-activated STAT proteins and the development of GH resistance (Schaefer et al., 2001; Sun et al., 2004; Mak and Cheung, 2007; Cheung et al., 2008). The gene discussed is GH1; the disease is chronic kidney disease.