JUN and acute kidney injury: Given that FABP4 was reported to modulate TLR4 signaling and JNK/c-Jun cascade in different pathological processes [27, 30], and combined with our findings, we speculated that a positive feedback loop might exist between FABP4 and TLR4/MyD88/JNK/c-Jun signaling, which further amplifies inflammatory response and cell apoptosis in septic AKI.