To confirm that the PXS‐5153A‐mediated inhibition of crosslinking seen in the in vitro assay would ensue in an in vivo setting, the CCl4 model of liver fibrosis—that can be LOXL2 dependent—was performed.13 Remarkably, mRNA levels of LOXL2 and LOXL3 were substantially increased upon 6‐weeks of CCl4 treatment (Figure 3A), which confirmed the suitability of the model for assessing the role of LOXL2/LOXL3. This evidence concerns the gene LOXL3 and Hepatic fibrosis.