It is suggested that direct targeting JNK or TGFβ1 may not be an effective therapeutic strategy for liver fibrosis as these two signaling molecules exert multifunctional effects on various biological processes including tissue homeostasis, cell proliferation and differentiation, and protein synthesis.[6, 51] Global knockout mice of TGFβ1 and JNK‐1/JNK‐2 double knockout mice are embryonic lethal.[53, 54] On the contrary, treatment with BMS309403 attenuated the BDL‐induced activation of JNK/c‐Jun and TGFβ1/Smad3 signaling while retained their basal activities. The gene discussed is JUN; the disease is Hepatic fibrosis.