MET and neoplasm: For instance, both IKKβ-deficient fibroblasts and TPL2-deficient myofibroblasts were found to secrete elevated levels of hepatocyte growth factor (HGF) [36,37], an important cytokine involved in tumor development and progression [39,40,41], and pharmacological inhibition of the HGF receptor (MET) could revert the phenotype caused by (myo)fibroblast-specific deletion of these targets [36,37].