GH resistance triggered by local production of cytokines can be attributed to a drop in GH receptor (GHR) expression via inhibition on GHR promoter activity (10–12) with parallel activation of SOCS expression (e.g., SOCS1, SOCS3, and CISH) (3, 12, 13), which can lead to failure in linear growth during childhood development (14) as well as muscle wasting, poor wound healing, cachexia, hepatic steatosis and insulin resistance in adult stage (14, 15). This evidence concerns the gene CISH and fatty liver disease.