FASN and hypertriglyceridemia: Clinical development of this drug class is also hindered by significant off-target toxicity (Katz et al., 2009; Kirchgessner et al., 2016), owing largely to activity of the LXRα isoform in the liver (Oosterveer et al., 2010), inducing hepatic lipogenesis and hypertriglyceridemia via activation of sterol regulatory element-binding protein-1 gene (SREBP-1), fatty acid synthase (FASN) and Cytochrome P450 Family 7 Subfamily A Member 1 (CYP7A1) (Schultz et al., 2000; Im and Osborne, 2011).