MDM2 amplification has been identified according to some data in up to 44% of patients with HCC.[10] It is assumed that MDM2 amplification may predict sensitivity to MDM2 inhibitors; however, currently available evidence is inconclusive.[11] At the time of referral to the CCTT the patient had metastatic disease to lungs and bones and subsequently received experimental therapy with sorafenib (200 mg orally twice a day), temsirolimus (15 mg intravenously weekly), and bevacizumab (10 mg/kg intravenously every 3 weeks), which did not match any molecular target. Here, MDM2 is linked to metastatic neoplasm.