FABP4 and Hepatic fibrosis: In the present study, evidence from both genetic ablation and pharmacological inhibition in animals demonstrates, for the first time, that A‐FABP is a key mediator of liver fibrosis by coordinating the crosstalk between LSECs and HSCs to initiate and perpetuate HSC activation, thus exaggerates the production of the fibrogenic cytokine TGFβ1 from HSCs.