Erlotinib treatment temporarily suppressed most of the investigated parameters on wild type mice but there was no difference between the control and the treated animals at the endpoint and similar to imatinib it was completely inefficient in the transgenic mice overexpressing TGFβ and in the therapeutic experiment Erlotinib successfully blocked the proliferation of ductular reaction in Nf2-/- mice [46], it also attenuated liver fibrosis in bile duct ligated rats and CCl4 treated mice [22]. Here, NF2 is linked to Hepatic fibrosis.