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. Here, TGFB1 is linked to Hepatic fibrosis.