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However, a recent randomized trial in patients treated with BOC, shows that RBV dose reduction and EPO use did not influence the SVR and were equally effective in managing anaemia whether HCV RNA was detectable or not [42]. Therefore, RBV dose reduction should be the first line approach in case of triple regimen-induced anaemia. Triple therapies with PIs are a major advance in the history of HCV treatment. Optimal patient selection is crucial to achieve high SVR rates with a reasonable safety profile. Real-life data on patients with cirrhosis have shown the benefit of triple therapy in the most difficult-to-treat patients. They also define the limits https://www.selleckchem.com/products/dabrafenib-gsk2118436.html of this treatment. Patients with cirrhosis, a platelet count https://www.selleckchem.com/products/sch772984.html should not be treated. Recent data have shown the benefits of the triple regimen with BOC in HCV patients with extrahepatic manifestations, in post liver transplantation HCV recurrence and in HIV-HCV co-infected patients. Optimizing BOC treatment includes optimizing the treatment design according to baseline characteristics, following optimal stopping rules, preventing DDIs and preventing and managing AEs. M. Bourli��re has served on the Speaker bureaus of Roche, Bristol Myers Squibb, GSK, Gilead, Merck, Janssen; Consultant: Roche, Bristol Myers Squibb, GSK, Gilead, Merck, Janssen, Boehringer Ingelheim, Vertex, Novartis and Abbvie. X. Adhoute, A. Wendt, C. Ansaldi, V. Oules and P. Castellani have no disclosures. ""Non-alcoholic fatty liver disease (NAFLD) is the main cause of chronic liver disease in the occidental world, being already the third cause of liver transplantation in the United States [1]. With the growing epidemic of obesity and because of the fact that we do not have an effective therapy, the burden of NAFLD will expectedly increase. As such, the search for new potential therapeutic targets is in the order of the day. Nuclear receptors (NR) are ligand-activated transcriptional factors that not only are major regulators of metabolism but also have intricate connections with circadian control explaining our cyclical behaviours regarding nutrient fate, as very comprehensively reviewed https://www.selleck.cn/products/z-vad-fmk.html in this number of Liver International [2]. In fact, the ability to adapt between fasting and fed states is crucial for survival, and when deregulated may promote obesity and its complications, such as diabetes mellitus and NAFLD [3]. Manipulating NR opens a vast field of investigation for the treatment of NAFLD. Several NR are known to be important players in obesity and liver disease. Pharmacological manipulation of some of those NR showed promising results in animal models of NAFLD, but proved rather disappointing when applied to clinical trials. One example is peroxisome proliferator-activated receptor (PPAR)-��, which by promoting fatty acid mitochondrial ��-oxidation and modulating lipoprotein metabolism decreases circulating triglycerides and hepatic steatosis/steatohepatitis in animal models [4].