LSECs are known as a determinant of liver fibrosis.[4] Upon chronic stimulation of damage factors, differentiated LSECs undergo capillarization which leads to the loss of its gatekeeper function for HSC activation.[4] As A‐FABP is mainly elevated in LSECs in liver fibrosis (Figure 2), we determined whether A‐FABP modulates LSEC capillarization. This evidence concerns the gene FABP4 and Hepatic fibrosis.