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. This evidence concerns the gene SMAD3 and cholestasis.