This was supported by another study, which indicated that there was a significant decrease in the expression of the JAK/STAT3 inhibitor, SOCS1, in IPF as compared to normal lung fibroblasts, which was correlated with increased COL1 expression by IPF lung fibroblasts (Shoda et al., 2007). This evidence concerns the gene STAT3 and idiopathic pulmonary fibrosis.