BMS309403 possesses multiple beneficial effects on various metabolic diseases in animal studies.[8] Global A‐FABP KO mice are also metabolic healthy.[8] The present findings support that inhibition of A‐FABP is an effective and relatively safe therapeutic strategy for liver fibrosis through suppressing the over‐activated JNK/c‐Jun and the subsequent TGFβ1/Smad3 signaling, which implicates that targeting A‐FABP may be an effective approach against liver fibrosis caused by different etiologies but not only restricted to cholestasis. The gene discussed is JUN; the disease is metabolic disease.