Furthermore, mutations at either V550 (a gatekeeper residue) or C552 (hinge-1 residue) in the kinase domain of fibroblast growth factor receptor 4 (FGFR4) prevent fisogatinib (a potent and selective FGFR4 inhibitor) from interacting with the FGFR4’s ATP binding site, resulting in acquired clinical resistance to fisogatinib in patients with HCC [64]. Here, FGFR4 is linked to hepatocellular carcinoma.