While PLX51107 and dinaciclib share a common metabolism via CYP3A4, other investigations examining BET inhibitors for treatment of liver cancer suggest hepatotoxicity is not merely a result of drug-drug interaction but reflects normal role of their respective targets in hepatocyte biology where BET proteins have a known role in hepatocyte proliferation in response to injury [77–79]. The gene discussed is DNER; the disease is liver cancer.