Various oncogenic inputs associated with HCC decreased as a result of ADAMTSL5 abrogation, such as MET, EGFR, PDGFRβ, IGF1Rβ and FGFR4 receptor tyrosine kinases, which were all expressed and/or phosphorylated to a lesser extent, showing the potential role of ADAMTSL5 in HCC drug resistance (194). The gene discussed is MET; the disease is hepatocellular carcinoma.