MET and hepatocellular carcinoma: The previous in vitro biochemical kinase assay demonstrated that VEGFRs, PDGFR, FGFRs, c‐MET, RET, Flt3, c‐KIT, and Raf kinase could be targeted by sorafenib.[23] Nevertheless, the expression of RAF was found to be lower in HCC than in paracarcinoma tissue.[24] VEGFR and FGFR were reported to be associated with the sorafenib response in HCC.[25, 26] In the current study, we demonstrated that MCB1 bound directly to FGFR1 or VEGFR3 and promoted the degradation of ubiquitinated FGFR1 or VEGFR3.