However, the fact that the pharmacological blockade of the growth hormone receptor reversed most of the main phenotypic characteristics of the TgC6hp55 mice (enhanced somatic growth, hepatic steatosis, increased adipocyte size etc.), suggests that the major actions of the hGH in mediating the TgC6hp55 phenotype are through this receptor, while the activation of the prolactin receptor plays a more secondary role. Here, PRLR is linked to fatty liver disease.