CEBPB and pulmonary fibrosis: Given the important role of RSK and its phosphorylation of C/EBPβ-Thr217 in the activation of liver myofibroblasts (hepatic stellate cell) [10],[22] and the suggested similarities between liver and lung fibrogenesis [1],[23], we hypothesized that a dominant negative, non-phosphorylatable transgenic C/EBPβ-Ala217 would block phosphorylation of C/EBPβ-Thr217 by RSK, preventing lung myofibroblast (LMF) activation and decreasing lung fibrosis after lung injury.